SUBSTITUTION REACTIONS OF THE MONOFUNCTIONAL GOLD(III) COMPLEX AND SULPHUR-DONOR BIOLOGICALLY IMPORTANT LIGANDS

Gold(III) complexes have found application in catalysis, materials science and medical inorganic chemistry. Considering that the right choice of inert ligands in the structure of Au(III) complexes is crucial for their properties and reactivity toward biomolecules, we have studied the substitution reactions between monofunctional Au(III) complex, [Au(Cl-Ph-tpy)Cl]Cl2 (Cl- Ph-tpy = 4′-(4-chlorophenyl)-2,2′:6′, 2″-terpyridine) and sulfur-donor biomolecules, glutathione (GSH) and L-methionine (L-Met), in 25 mM Hepes buffer (pH = 7.2) and 40 mM NaCl. The reactions were followed under the pseudo-first-order conditions as a function of ligand concentration and temperature, using the stopped-flow technique. Calculations were made by Microsoft Excel 2019 and Origin2019b 64Bit. Observed kinetics traces follow a single exponential function, suggesting that the process of the substitution undergoes as one reversible step. Also, L-Met was more reactive than GSH. This order is related to the positive inductive effect of the methyl group, which increases the nucleophilicity of the thioether. According to the values of the activation parameters, the reactions follow an associative model. These results demonstrate the strong connection between the reactivity of Au(III) complexes and the structural and electronic characteristics of the biologically important ligands.

A harmonic analysis of exponential decay

We analyse the decay of a single exponential function and develop an algorithm to determine the exponent and the constant, C, (C exp(-kt)) associated with this function . In essence this approach involves `transforming' exponential functions into harmonic functions. This manoeuvre allows techniques that are used to analyse harmonic functions to be used to characterise decaying exponential functions.

Coordinated control of volume regulatory Na+/H+ and K+/H+ exchange pathways in Amphiuma red blood cells

The Na+/H+ and K+/H+ exchange pathways of Amphiuma tridactylum red blood cells (RBCs) are quiescent at normal resting cell volume yet are selectively activated in response to cell shrinkage and swelling, respectively. These alkali metal/H+ exchangers are activated by net kinase activity and deactivated by net phosphatase activity. We employed relaxation kinetic analyses to gain insight into the basis for coordinated control of these volume regulatory ion flux pathways. This approach enabled us to develop a model explaining how phosphorylation/dephosphorylation-dependent events control and coordinate the activity of the Na+/H+ and K+/H+ exchangers around the cell volume set point. We found that the transition between initial and final steady state for both activation and deactivation of the volume-induced Na+/H+ and K+/H+ exchange pathways in Amphiuma RBCs proceed as a single exponential function of time. The rate of Na+/H+ exchange activation increases with cell shrinkage, whereas the rate of Na+/H+ exchange deactivation increases as preshrunken cells are progressively swollen. Similarly, the rate of K+/H+ exchange activation increases with cell swelling, whereas the rate of K+/H+ exchange deactivation increases as preswollen cells are progressively shrunken. We propose a model in which the activities of the controlling kinases and phosphatases are volume sensitive and reciprocally regulated. Briefly, the activity of each kinase-phosphatase pair is reciprocally related, as a function of volume, and the volume sensitivities of kinases and phosphatases controlling K+/H+ exchange are reciprocally related to those controlling Na+/H+ exchange.

Relaxation of Phonons in Classical MD Simulation

We propose a novel technique of molecular dynamics simulation to evaluate the relaxation time of phonons in solids for investigation of solid heat conductivity. The basic idea is to observe relaxation behavior of the power spectrum of atomic velocities after energetically stimulating modes in a specific frequency region. The transient entropy S(t) is defined with the power spectrum based on non-equilibrium statistical mechanics to quantitatively evaluate the relaxation speed. In this paper, two example systems are shown: a Lennard-Jones model crystal and a silicon crystal. For both systems, we found that the observed S(t) is well fitted to a single exponential function, from which we can obtain a frequency-dependent relaxation time.

14C Level At Mt Chiak and Mt Kyeryong in Korea

We have observed A14C concentrations in the northern hemisphere temperate region in the bomb pulse period, using cross-dated tree ring samples. The tree-ring samples were taken from one 70-year-old and two 50-year-old red pines (Pinus densiflora) on Mt Chiak, Korea and from a 50-year-old red pine (Pinus densiflora) on Mt Kyeryong, Korea. Twenty-two tree-ring samples from four red pines ranging from 1950 to 2000 AD were pretreated to obtain holo-cellulose, combusted to CO2 by an element analyzer (EA) and converted to graphite for δ14C measurement using the accelerator mass spectrometry (AMS) facility at Seoul National University. Our results for δ14C showed good agreement with those measured by other researchers at similar latitudes. The observed steady decrease of δ14C from 1965 to 2000 AD is described by a single exponential function with a lifetime τ = 15.99 ± 0.43 yr. This lifetime is similar to that of the high-latitude region in Europe.

Persistent Na+ Current and Ca2+ Current Boost Graded Depolarization of Rat Retinal Amacrine Cells in Culture

Retinal amacrine cells are depolarized by the excitatory synaptic input from bipolar cells. When a graded depolarization exceeds the threshold level, trains of action potentials are generated. There have been several reports that both spikes and graded depolarization are sensitive to tetrodotoxin (TTX). In the present study, we investigated the contribution of voltage-gated currents to membrane depolarization by using rat GABAergic amacrine cells in culture recorded by the patch-clamp method. Injection of a negative current induced membrane hyperpolarization, the waveform of which can be well fitted by a single exponential function. Injection of positive current depolarized the cell, and the depolarization exceeded the amplitude expected from the passive properties of the membrane. The boosted depolarization sustained after the current was turned off. Either 1 μM TTX or 2 mM Co2+ suppressed the boosted depolarization, and co-application of TTX and Co2+ blocked it completely. Under the voltage clamp, we identified a transient Na+ current (fast I Na), a TTX-sensitive persistent current that reversed the polarity near the equilibrium potential of Na+ ( I NaP), and three types of Ca2+ currents ( I Ca), L, N, and the pharmacological agent-resistant type (R type). These findings suggest that the I NaP and I Ca of amacrine cells boost depolarization evoked by the excitatory synaptic input, and they may aid the spread of electrical signals among dendritic arbors of amacrine cells.

Novel properties of hepatic canalicular reduced glutathione transport revealed by radiation inactivation

Transport of GSH at the canalicular pole of hepatocytes occurs by a facilitative carrier and can account for ∼50% of total hepatocyte GSH efflux. A low-affinity unit with sigmoidal kinetics accounts for 90% of canalicular transport at physiological GSH concentrations. A low-capacity transporter with high affinity for GSH has also been reported. It is not known whether the same or different proteins mediate low- and high-affinity GSH transport, although they do differ in inhibitor specificity. The bile of rats with a mutation in the canalicular multispecific organic anion transporter (cMOAT or MRP-2, a 170-kDa protein) is deficient in GSH, implying that cMOAT may transport GSH. However, transport of GSH in canalicular membrane vesicles (CMV) from these mutant rats remains intact. We examined the functional size of the two kinetic components of GSH transport by radiation inactivation of GSH uptake in rat hepatic CMV. High-affinity transport of GSH was inactivated as a single exponential function of radiation dose, yielding a functional size of ∼70 kDa. In contrast, low-affinity canalicular GSH transport exhibited a complex biexponential response to irradiation, characterized by an initial increase followed by a decrease in GSH transport. Inactivation analysis yielded a ∼76-kDa size for the low-affinity transporter. The complex inactivation indicated that the low-affinity transporter is associated with a larger protein of ∼141 kDa, which masked ∼80% of the potential transport activity in CMV. Additional studies, using inactivation of leukotriene C4 transport, yielded a functional size of ∼302 kDa for cMOAT, indicating that it functions as a dimer.

Twenty Years of Atmospheric 14Co2 Observations At Schauinsland Station, Germany

We present and discuss quasi-continuous long-term 14CO2 observations from the continental background station Schauinsland (48°N, 8°E, 1205 m asl, Black Forest, southern Germany). The observed steady decline of atmospheric 14CO2 from 1977 to 1996 can be described by a single exponential function with an e-folding time of (16.3 ± 0.2) yr. Summer means (May to August) in atmospheric 14CO2 at Schauinsland compare within Δ14C = ±4‰ with measurements made on individual rings from a tree grown in the near vicinity of the Schauinsland site. Both data sets are slightly depleted by up to 5‰ if compared to maritime background measurements of atmospheric 14CO2 made at Izaña, Tenerife. This is due to the influence of fossil fuel CO2 emissions over the European continent as well as generally in mid latitudes of the Northern Hemisphere. δ13C analyses from the Schauinsland samples show mean seasonal variations with an amplitude of ±0.4‰, caused by atmosphere-biosphere exchange, and a mean decrease from 1977 to 1996 of δ13C = −0.017‰ yr−1. This trend is mainly due to an increasing quantity of fossil fuel CO2 in the atmosphere, depleted in 13C/12C ratio, and compares well to trends measured at other stations in mid-to-high northern latitudes.

Fast approximate solutions of transient EM response to a target buried beneath a conductive overburden

We derive fast transient electromagnetic (TEM) solutions for a thin‐plate conductive target buried in a resistive host rock overlain by thin conductive overburden. For this model, the total TEM field is composed of the overburden response, which is known analytically, and the target response that is approximated by a wire loop. Thus the transient response of the target in free space is approximated with a single exponential function. The interaction between the target and the overburden is approximated by convolving the overburden‐delayed driving field with the exponential function. The target response is then computed from the wire loop by the Biot‐Savart law in free space, thus neglecting the second overburden‐delay effect. Including the second overburden‐delay effect does not yield significantly improved results. The approximate solutions agree reasonably well with scale model and numerical results, but their computation is more than 100 times faster than conventional methods and can be easily done on a small personal computer.

Calcium-dependent inactivation of the calcium current activated upon hyperpolarization of Paramecium tetraurelia.

The Ca2+ current activated upon hyperpolarization of Paramecium tetraurelia decays over a period of 150-200 ms during sustained steps under voltage clamp. At membrane potentials between -70 and approximately -100 mV, the time course of this inactivation is described by a single exponential function. Steps negative to approximately -100 mV elicit currents that decay biexponentially, however. Three lines of evidence suggest that this current's inactivation is a function of intracellular Ca2+ concentration rather than membrane potential: (a) Comparing currents with similar amplitudes but elicited at widely differing membrane potentials suggests that their time course of decay is a sole function of inward current magnitude. (b) The extent of current inactivation is correlated with the amount of Ca2+ entering the cell during hyperpolarization. (c) The onset and time course of recovery from inactivation can be hastened significantly by injecting cells with EGTA. We suggest that the decay of this current during hyperpolarization involves a Ca(2+)-dependent pathway.