Anomalies In Kinetics Research Articles

816 UNA Diagnosi . . . Incidentale

Hypertrophic cardiomyopathy (HCM) is the most frequent genetic disease of the myocardium, with a prevalence of 1:500 cases in the general population. The salient feature is a hypertrophy, symmetrical or not, of the walls of the left ventricle (mainly the septum, but also less typical locations, such as the apex or the infero-lateral wall), not linked to abnormal load conditions. HCM is mostly an autosomal dominant inherited disease with incomplete penetrance and variable expressivity, mainly linked to mutations in genes coding for sarcomeric proteins. Several studies have shown an up-regulation of the ACE-2 gene, perhaps indicative of a compensatory anti-hypertrophic and anti-fibrotic response of the myocardium, in hypertrophic cardiomyopathy. Being the ACE-2 receptor target of the Sars-CoV-2 virus, these patients may have an increased risk of infection and a worse outcome. A 47-year-old man, with no known comorbidities, was hospitalized in our Emergency Medicine Department for bilateral Sars-CoV-2 pneumonia. Noninvasive mechanical ventilation c-PAP (FiO2 60%, PEEP 7.5 cmH20) was started for hypoxemic respiratory failure and an ECG showed diffuse ventricular repolarization abnormalities suggestive of left overload (asymmetric negative T waves V4 to V6, in I, II and aVL, flat in aVF. Figure 1), with a deep Q wave in III. The patient was asymptomatic for chest pain and equivalents and D-dimer and indices of myocardionecrosis were normal. Echocardiographic evaluation was performed, with evidence of marked asymmetric concentric hypertrophy of the left ventricle (interventricular septum: 16 mm), without significant anomalies in segmental kinetics, noteworthy valvulopathies and pericardial effusion. The family and personal medical history were negative for syncope, sudden cardiac death and resuscitated cardiac arrest and the estimated risk of sudden cardiac death at five years (HCM Risk-SCD) was <4% (1.33%). The diagnostic hypothesis of non-obstructive hypertrophic cardiomyopathy was advanced. During hospitalization, ECG monitoring showed no sustained ventricular arrhythmias and the patient remained asymptomatic for dyspnoea, chest pain and equivalents. Subsequent echocardiograms showed no new changes. A progressive weaning from oxygen support was carried out and, after thirty days, the patient was discharged to home fiduciary isolation, with optimal cardiological therapy and indication to study with cardiac magnetic resonance to the negativization of the nasal swab for Sars-CoV-2. MRI, performed about two months later, confirmed the suspicion of hypertrophic cardiomyopathy, with no signs of late enhancement in T1-weighted sequences (Figure 2). The patient was then referred to a genetic study and cardiological follow-up, still in progress. 816 Figure 1816 Figure 1

527 An incidental diagnosis in a patient with SARS-CoV-2 pneumonia

Hypertrophic cardiomyopathy (HCM) is the most frequent genetic disease of the myocardium, with a prevalence of 1:500 cases in the general population. The salient feature is a hypertrophy, symmetrical or not, of the walls of the left ventricle (mainly the septum, but also less typical locations, such as the apex or the infero-lateral wall), not linked to abnormal load conditions. HCM is mostly an autosomal dominant inherited disease with incomplete penetrance and variable expressivity, mainly linked to mutations in genes coding for sarcomeric proteins. Several studies have shown an up-regulation of the ACE-2 gene, perhaps indicative of a compensatory anti-hypertrophic and anti-fibrotic response of the myocardium, in hypertrophic cardiomyopathy. Being the ACE-2 receptor target of the SARS-CoV-2 virus, these patients may have an increased risk of infection and a worse outcome.A 47-year-old man, with no known comorbidities, was hospitalized in our Emergency Medicine Department for bilateral SARS-CoV-2 pneumonia. Noninvasive mechanical ventilation c-PAP (FiO2 60%, PEEP 7.5 cmH2O) was started for hypoxemic respiratory failure and an ECG showed diffuse ventricular repolarization abnormalities suggestive of left overload (asymmetric negative T waves V4–V6, in I, II, and aVL, flat in aVF. Figure 1), with a deep Q wave in III. The patient was asymptomatic for chest pain and equivalents and D-dimer and indices of myocardionecrosis were normal. Echocardiographic evaluation was performed, with evidence of marked asymmetric concentric hypertrophy of the left ventricle (interventricular septum: 16 mm), without significant anomalies in segmental kinetics, noteworthy valvulopathies, and pericardial effusion. The family and personal medical history were negative for syncope, sudden cardiac death, and resuscitated cardiac arrest and the estimated risk of sudden cardiac death at 5 years (HCM Risk-SCD) was <4% (1.33%). The diagnostic hypothesis of non-obstructive hypertrophic cardiomyopathy was advanced. During hospitalization, ECG monitoring showed no sustained ventricular arrhythmias and the patient remained asymptomatic for dyspnoea, chest pain, and equivalents. Subsequent echocardiograms showed no new changes. A progressive weaning from oxygen support was carried out and, after 30 days, the patient was discharged to home fiduciary isolation, with optimal cardiological therapy and indication to study with cardiac magnetic resonance to the negativization of the nasal swab for SARS-CoV-2. MRI, performed about 2 months later, confirmed the suspicion of hypertrophic cardiomyopathy, with no signs of late enhancement in T1-weighted sequences (Figure 2). The patient was then referred to a genetic study and cardiological follow-up, still in progress.

Spin kinetics of liquid 3He in an aerogel–DyF3 nanoparticle system

The pulsed NMR method was used to study the spin kinetics of liquid 3Не in a sample of oriented Al2O3 aerogel, containing DyF3 nanoparticles with an average size of 5 nm, at temperatures of 1.5−3 K. DyF3 is a dipole dielectric ferromagnet with a phase transition temperature of TC = 2.55 K, while the diamagnetic ordered Al2O3 aerogel is used as a magnetic diluting agent to ensure the optimal conditions for observing the 3Не nuclear magnetic resonance in this system. No anomalies in the spin kinetics of 3Не contacting with this sample that could be related to the phase transition have been observed. A method for adding paramagnetic impurities to aerogel was proposed.

Anomalies in radiation-collisional kinetics of Rydberg atoms induced by the effects of dynamical chaos and the double Stark resonance

Radiative and collisional constants of excited atoms contain the matrix elements of the dipole transitions and when they are blocked one can expect occurring a number of interesting phenomena in radiation-collisional kinetics. In recent astrophysical studies of IR emission spectra it was revealed a gap in the radiation emitted by Rydberg atoms (RA) with values of the principal quantum number of n≈10. Under the presence of external electric fields a rearrangement of RA emission spectra is possible to associate with manifestations of the Stark effect. The threshold for electric field ionization of RA is E≈3·104 V/cm for states with n>10. This means that the emission of RA with n≥10 is effectively blocked for such fields. In the region of lower electric field intensities the double Stark resonance (or Förster resonance) becomes a key player. On this basis it is established the fact that the static magnetic or electric fields may strongly affect the radiative constants of optical transitions in the vicinity of the Föster resonance resulting, for instance, in an order of magnitude reduction of the intensity in some lines. Then, it is shown in this work that in the atmospheres of celestial objects lifetimes of comparatively long-lived RA states and intensities of corresponding radiative transitions can be associated with the effects of dynamic chaos via collisional ionization. The Föster resonance allows us to manipulate the random walk of the Rydberg electron (RE) in the manifold of quantum levels and hence change the excitation energies of RA, which lead to anomalies in the IR spectra.

Anomalies in segregation kinetics of solutes under tensile stress in heat resistant steel

In heat resistant steels, tensile stress accelerates the decomposition of preexisting smaller carbides and the growth of larger carbides. Consequently, the dissolved carbon is enriched in the matrix during the decomposition. Under the tensile stress, the massive diffusion of the enriched carbon results in more active segregation to the grain boundary/carbide interfaces for the growth of the larger carbides than the carbide-free grain boundaries. The segregation kinetics of carbon forms a convex profile during the growth process of carbides. A concave segregation profile of chromium corresponds to the convex profile of carbon. This is attributed to the diffusivity of chromium much lower than that of carbon which makes the chromium as the rate-controlling factor for the carbide growth. Due to the repulsive segregation behavior between carbon and phosphorus, the concave segregation profile of phosphorus results from the convex segregation profile of carbon formed during the active carbide growth. A convex segregation profile of sulfur is also formed owing to the formation reaction of MnS particles, but it is independent of the segregation behaviors of the other solutes.

Precipitation related anomalies in kinetics of phosphorus grain boundary segregation in low alloy steels

It has been shown that particles of M 6C in Cr–Mo–V low alloy steels can influence phosphorus grain boundary segregation in a similar manner to Laves phase particles in 12CrMoV steel. The influence of these particles arises from their ability to dissolve non- metallic elements such as phosphorus and silicon. As phosphorus is progressively segregated to the grain boundaries during prolonged ageing, the precipitation of M 6C particles leads to an anomalous decrease in the phosphorus grain boundary concentration as the ageing time is extended. This phenomenon originally observed for the Laves phase in long-term aged 12CrMoV steel at temperatures of 753, 773, and 803 K has now been observed for M 6C carbide in a 2.5Cr–0.4Mo–0.25V low alloy steel aged at 853 K.

Anomalies in the slow polarization kinetics of a ferroelectric relaxor in the temperature region of a diffuse phase transition

It is shown experimentally in the specific example of Cr-doped barium-strontium niobate that the anomalies in the infralow-frequency dielectric properties characteristic of a ferroelectric relaxor persist over the whole temperature region of the diffuse phase transition and decrease gradually with increasing temperature. Experimental data are presented on the anomalous quasi-static dielectric hysteresis loops, the slow polarization kinetics, and the anomalously broad energy-distribution spectra of potential barriers. The anomalies are a signature and a quantitative measure of the structural disorder typical of a relaxor.

Anomalies in kinetics of hydrogen evolution from austenitic stainless steel from 300 to 1000 °C

The rate of rise method was arranged for monitoring the kinetics of hydrogen evolution from austenitic stainless steel (AISI 304) samples, inductively heated in the range from 300 to 1000 °C. After each heating cycle, the accumulated gases were analyzed by quadrupole mass spectroscopy and quantity of evolved hydrogen was determined. Three sample types were studied: “only cleaned,” hydrogen annealed (1050 °C), and vacuum annealed (950 °C). Below 800 °C, the effect of pretreatment was manifested very differently in kinetics. Fast release of approximately 2×1019 atoms H cm−3 from hydrogen annealed samples was recorded which was close to published data of solubility. By increasing the temperature above 800 °C for a prolonged time, much more hydrogen evolved from all sample types. The equivalent concentration change varied from 4 to 9×1019 atoms H cm−3, but the measurements were ceased before the “totally outgassed state” was reached. By repeated annealing of two samples in high vacuum, the rest of the hydrogen was again partially extracted and partially redistributed to the sites, from which it was easily released after intermediate cooling down. There is a lack of data in the literature about the amount and evolution kinetics of the trapped or tightly bound hydrogen. The present findings differ from existing theoretical models of outgassing and may explain the reason for the inefficiency of thermal treatment methods to prepare stainless steel for extreme high vacuum application.

Anomalies in the growth kinetics of Saccharomyces cerevisiae strains in aerobic chemostat cultures

Aerobic glucose-limited chemostat cultivations were conducted with Saccharomyces cerevisiae strains NRRL Y132, ATCC 4126 and CBS 8066, using a complex medium. At low dilution rates all three strains utilised glucose oxidatively with high biomass yield coefficients, no ethanol production and very low steady-state residual glucose concentrations in the culture. Above a threshold dilution rate, respiro-fermentative (oxido-reductive) metabolism commenced, with simultaneous respiration and fermentation occurring, which is typical of Crabtree-positive yeasts. However, at high dilution rates the three strains responded differently. At high dilution rates S. cerevisiae CBS 8066 produced 7–8 g ethanol L−1 from 20 g glucose L−1 with concomitant low levels of residual glucose, which increased markedly only close to the wash-out dilution rate. By contrast, in the respiro-fermentative region both S. cerevisiae ATCC 4126 and NRRL Y132 produced much lower levels of ethanol (3–4 g L−1) than S. cerevisiae CBS 8066, concomitant with very high residual sugar concentrations, which was a significant deviation from Monod kinetics and appeared to be associated either with high growth rates or with a fermentative (or respiro-fermentative) metabolism. Supplementation of the cultures with inorganic or organic nutrients failed to improve ethanol production or glucose assimilation. Journal of Industrial Microbiology & Biotechnology (2000) 24, 231–236.

Thermomechanical Properties of Radiation-Modified Polyethylene/Ethylene-Propylene-Diene Copolymer/Liquid-Crystalline Copolyester Blends

Radiation-modified blends of high-density polyethylene (PE) with ethylene-propylene-diene copolymer (EPDM; 10-65 wt.%) and thermotropic liquid-crystalline polymer (LCP; 10 wt.%) were investigated. The LCP was a liquid-crystalline copolyester of 40% poly(ethylene terephthalate) with 60% 4-hydroxybenzoic acid. The constituents were blended using a circular extruder, the specimens were prepared by compression molding and irradiated by 60Co γ-radiation up to 200 kGy. Mechanical, thermal, and morphological properties in wide temperature range were investigated for the irradiated and non-irradiated specimens. The effects of irradiation on the thermomechanical behaviour of the PE matrix are discussed. The LCP addition significantly affected the stress-strain behaviour of PE at temperatures above its melting point resulting in some anomalies in kinetics of formation of thermorelaxation stresses, which arise if the material is previously oriented. Thermosetting properties (thermorelaxation stresses and residual setting stresses under conditions of isometric heating and cooling) of the PE/EPDM/LCP blends crosslinked by irradiation and then oriented were also established. The results obtained suggest that such ternary blends improve the application properties of irradiated polyethylene and obtain useful thermosetting materials.

Do inherited prothrombotic factors have a role in myocardial infarction with normal coronary arteriogram?

Dear Sir, several inherited prothrombotic anomalies, such as antithrombin III, protein C or protein S deficiencies, factor V Leiden and factor II variant, have been established as risk factors for venous thromboembolism [1]. By contrast, involvement of inherited prothrombotic anomalies in coronary thrombosis is still a matter of debate [2,3]. We have conducted a retrospective study to explore the prevalence of inherited prothrombotic factors in an uncommon population of acute myocardial infarction without any evidence of atheroma on coronary arteriogram. Two hundred and three patients aged 24–40 (mean ± SD: 32 ± 5) years admitted to the Cardiology Department, Nantes University Hospital, were diagnosed with a first acute myocardial infarction between 1 January 1986 and 1 May 1997. Criteria for myocardial infarction were defined by evidence of symptoms, elevated enzymes, electrocardiographic changes and localized anomalies in ventricular kinetics. Only patients without any evidence of atheroma on coronary arteriogram were selected (n = 26). All were alive at the time of the study. Fourteen patients (12 males, two females) out of 26 were recruited. Of the 12 remaining patients three were excluded because of an acquired cause of thrombophilia (two nephrotic syndrome, one thrombocytosis), eight could not be located and one refused to participate. The 14 enrolled patients were interviewed with about atherosclerotic factors preceding acute myocardial infarction: all but one had at least one identified risk factor with special representation of smokers (71%) and hypercholesterolaemia (57%) (mean ± SD: 2.92 ± 0.46 g L−1). Blood samples were obtained from the antecubital vein between 3 months and 10 years after the myocardial infarction. Samples were sent blinded to the laboratory. The presence of a factor II variant (20210 A allele) or a factor V Leiden (R506Q) was determined using a specific polymerase chain amplification and Hind III digestion [4]. For protein C and protein S, activities were determined by clotting assays and antigenic values using an ELISA test (Diagnostica Stago, France). Antithrombin III activity was measured using amidolytic substrates (Diagnostica Stago). Normal values of protein C and protein S were defined as between 70 and 130%. The same biological assays were also performed in a sex- and age-matched control group of healthy subjects (n = 28). Results demonstrated an increased prevalence of genetic variants in patients with myocardial infarction as compared to the control group (Fisher's exact test; P < 0.02). Thirty-six per cent of the cases (5/14) carried an inherited prothrombotic factor: three males were heterozygous for factor V Leiden; protein C deficiency was found in one female (activity: 58%; antigen: 63%), and protein S deficiency in the other female (activity: 39%; antigen: 47%). None of the patients carried a factor II mutation or antithrombin III deficiency. Only one healthy subject from the control group carried an inherited prothrombotic factor (heterozygous for factor V Leiden). This is the first study to raise inherited prothrombotic disorders as potential risk factors for coronary thrombosis in patients with normal coronary arteriogram. It legitimates a large-scale prospective study (to be conducted) that will further elucidate the deleterious role of inherited prothrombotic factors in such a population.

Do inherited prothrombotic factors have a role in myocardial infarction with normal coronary arteriogram?

Dear Sir, several inherited prothrombotic anomalies, such as antithrombin III, protein C or protein S deficiencies, factor V Leiden and factor II variant, have been established as risk factors for venous thromboembolism [1]. By contrast, involvement of inherited prothrombotic anomalies in coronary thrombosis is still a matter of debate [2, 3]. We have conducted a retrospective study to explore the prevalence of inherited prothrombotic factors in an uncommon population of acute myocardial infarction without any evidence of atheroma on coronary arteriogram. Two hundred and three patients aged 24–40 (mean ± SD: 32 ± 5) years admitted to the Cardiology Department, Nantes University Hospital, were diagnosed with a first acute myocardial infarction between 1 January 1986 and 1 May 1997. Criteria for myocardial infarction were defined by evidence of symptoms, elevated enzymes, electrocardiographic changes and localized anomalies in ventricular kinetics. Only patients without any evidence of atheroma on coronary arteriogram were selected (n = 26). All were alive at the time of the study. Fourteen patients (12 males, two females) out of 26 were recruited. Of the 12 remaining patients three were excluded because of an acquired cause of thrombophilia (two nephrotic syndrome, one thrombocytosis), eight could not be located and one refused to participate. The 14 enrolled patients were interviewed with about atherosclerotic factors preceding acute myocardial infarction: all but one had at least one identified risk factor with special representation of smokers (71%) and hypercholesterolaemia (57%) (mean ± SD: 2.92 ± 0.46 g L−1). Blood samples were obtained from the antecubital vein between 3 months and 10 years after the myocardial infarction. Samples were sent blinded to the laboratory. The presence of a factor II variant (20210 A allele) or a factor V Leiden (R506Q) was determined using a specific polymerase chain amplification and Hind III digestion [4]. For protein C and protein S, activities were determined by clotting assays and antigenic values using an ELISA test (Diagnostica Stago, France). Antithrombin III activity was measured using amidolytic substrates (Diagnostica Stago). Normal values of protein C and protein S were defined as between 70 and 130%. The same biological assays were also performed in a sex- and age-matched control group of healthy subjects (n = 28). Results demonstrated an increased prevalence of genetic variants in patients with myocardial infarction as compared to the control group (Fisher's exact test; P < 0.02). Thirty-six per cent of the cases (5/14) carried an inherited prothrombotic factor: three males were heterozygous for factor V Leiden; protein C deficiency was found in one female (activity: 58%; antigen: 63%), and protein S deficiency in the other female (activity: 39%; antigen: 47%). None of the patients carried a factor II mutation or antithrombin III deficiency. Only one healthy subject from the control group carried an inherited prothrombotic factor (heterozygous for factor V Leiden). This is the first study to raise inherited prothrombotic disorders as potential risk factors for coronary thrombosis in patients with normal coronary arteriogram. It legitimates a large-scale prospective study (to be conducted) that will further elucidate the deleterious role of inherited prothrombotic factors in such a population.

Effects of orientation on the transport of d‐limonene in polypropylene

AbstractKinetics and equilibria of sorption and desorption of d‐limonene in three polypropylene films (unoriented polypropylene [UN], uniaxially oriented polypropylene [UA], and biaxially oriented polypropylene [BA]) were studied at 30°C and various penetrant activities. The weight percent uptake of a saturated vapor of limonene in UN, BA, and UA films ranged ranged from 12.5 to 19.0%. The kinetics of sorption of a saturated vapor of limonene in these polymers exhibits an increasing tendency toward Fickian transport as the degree of orientation increases, with the highly oriented BA approaching a Fickian response. As the penetrant activity is lowered, sorption kinetics tends to show a Fickian response more closely even for the UN and the UA films. Desorption of limonene from the three samples appears to be Fickian and considerably faster than sorption in the initial stages; however, the process decelarates after roughly half of the penetrant has desorbed. Subsequent exposure of the three oriented films to a saturated vapor of limonene resulted in identical sorption kinetics, suggesting the absence of crazing or other irreversible damage often associated with anomalous sorption in glassy polymers. These results illustrate that the concentration dependent anomalies in kinetics of sorption of a large penetrant such as limonene in the unoriented polypropylene film may be influenced by orientation to yield Fickian transport even at the highest external surface concentration. Thus, the orientation processes appear to affect large‐scale swelling‐induced relaxations to a larger degree than it does the diffusional processes which are dependent on smaller‐scale segmental motions. © 1995 John Wiley &amp; Sons, Inc.

Anomalies in surface kinetics caused by isotope dependent compression and phonon stiffening of molecular hydrogen monolayers on a transition metal surface.

We have investigated the layerwise growth and the coverage-dependent sticking coefficients of ${\mathrm{H}}_{2}$ and ${\mathrm{D}}_{2}$ on the (1\ifmmode\times\else\texttimes\fi{}1)H/Ru(001) surface at \ensuremath{\sim}5 K by precise thermal desorption spectrometry. Strong compression of the first layer compared to the higher ones (by 22% for ${\mathrm{H}}_{2}$, 12% for ${\mathrm{D}}_{2}$) is observed. Desorption energies and sticking coefficients drop precipitously in the compression range. We explain all these effects by the large, mass-dependent zero-point widths of these molecules in the layers, with consequent high compressibilities and stiffening-induced decrease of collisional energy transfer.

Interphotoreceptor Retinoid Binding Protein (IRBP) Enhances Rhodopsin Regeneration in the Experimentally Detached Retina

Results obtained in a previous study showed that, compared with a normal eyecup preparation, the amount of rhodopsin regenerated and the rate at which it was resynthesized after bleaching were reduced by about 50% when the skate retina was detached from its pigment epithelium (RPE) and replaced immediately on the apical surface of the RPE (Sun and Ripps, 1992). In the present study, these observations have been extended to preparations in which the detachment procedure was performed under fluid in order to dilute the IRBP content of the interphotoreceptor matrix. The goal initially was to determine whether lowering the IRBP concentration of the subretinal space affected the regenerative process. Using fundus reflectomerry, it was found that allowing fluid to enter the subretinal space exposed by the detachment procedure caused profound deficits in both the rate and amount of rhodopsin that regenerated after bleaching. Results obtained with SDS-PAGE and immunohistochemistry showed that the molecular weight of the IRBP extracted from the skate retina is similar to that of many other vertebrate species, and that antibodies prepared against mammalian IRBP react with epitopes on skate IRBP within the interphotoroceptor matrix. Accordingly, it was investigated whether it is possible to reverse the detachment-induced anomalies in rhodopsin kinetics by introducing ligand-free IRBP purified from bovine retina to the subretinal space. Again using fundus reflectometry, it was found that instilling 5 μM of a 130 μM IRBP solution between the neural retina and the RPE increased significantly the rate of regeneration, and more than doubled the amount of rhodopsin reformed in darkness.

Anomalies in the polymerization kinetics of 4-dimethylaminostyrene initiated with trichloracetic acid in nitrobenzene

The relative permittivities ( ϵ r 20) of 4-dimethylaminostyrene (I) and of 0.5–3.0 M solutions of N, N-dimethyl-4-toluidine (DMT) were measured in nitrobenzene (NB) and in a mixture of NB with diisopropyl ether (NB + E), the DMT solutions modelled those of I. An increase in [DMT] from 0.5 to 3.0 M caused a decrease in ϵ r 20 from 32.3 to 18.3 in NB, while only from 20.8 to 18.3 in (NB + E) at fixed [NB]. The great difference between the ϵ r 20 of 0.5 and 3.0 M DMT solutions in NB explains the previously observed drop in the percentage rate of polymerization ( R P) of I, in NB initiated with CCl 3COOH, with increasing [I] o. In (NB + E) mixture with fixed [NB], the percentage R P and the limiting viscosity number [ν] of polyl increase with increasing [I] o. The observed dependences of both R P (in Msec −1) and [ν] on [I] 0 confirm the validity of the suggested polymerization scheme for I initiated with CCl 3COOH, and make possible determination of the characteristics of the elementary polymerization reactions.

Cation effects on the fluorescence of isolated chloroplasts.

At room temperature, the fluorescence of chloroplasts in vivo and in vitro originates nearly exclusively from the chlorophyll of the oxygen evolving system II of the photosynthetic apparatus. The yield and the kinetics of this light emission are closely coupled to the primary photochemical events of photosystem II. Fluorescence studies, therefore, have contributed much to our knowledge about the water oxidizing photoact. According to Duysens and Sweers i(3) the fluorescence yield is determined by the oxidation state of the primary electron acceptor Q: when Q is oxidized, the fluorescence is quenched and, consequently, a low yield is observed; since reduced Q1(Q-) does not quench, a maximal fluorescence yield indicates a complete reduction of the electron acceptor pools containing Q. Several anomalies in the fluorescence kinetics of intact algae have led to the assumption of an non-homogeneous pool Q containing, even after the primary activation step (8), active and inactive oxidants Qa and Qi' (1,2, 4,12). Both forms of Q are thought to quench the fluorescence in their oxidized states, albeit with slightly different effectiveness. A photoreduction of the total pool Q requires an activation of any Qi' to Qa, which according to some authors (1,4,12) is sensitized by photosystem I. In this communication, we wish to report on an overriding influence of the ionic environment on the fluorescence yield of isolated chloroplasts. It will be shown that the fluorescence yield can be changed at will simply by varying the composition of the suspension medium. Accordingly, the fluorescence yield may possibly be governed not only by the oxidation state olf the Q-pool, but also by ion induced structural changes.

Introduction to the Symposium on Anomalies in Reaction Kinetics.

Introduction to the Symposium on Anomalies in Reaction Kinetics.

Spirited Discussions Characterize Symposium on Anomalies in Reaction Kinetics

Spirited Discussions Characterize Symposium on Anomalies in Reaction Kinetics