Net Entry Research Articles

Entry and competition in banking

Economic theory suggests that, ceteris paribus, new entry of firms will increase rivalry in a market. This study analyzes 184 banking markets to determine whether net market entry over the period 1968–1974 (entry less exist) influenced rivalry (mobility and turnover among top five firms). Results of a multivariate regression analysis indicate no relationship between entry and rivalry. Two possible explanations for this somewhat surprising finding are: (1) new entry into banking markets is typically on a relative small scale, and (2) if potential competition had been an effective factor prior to entry in some of the markets where net entry took place, the potential effect of new entry on rivalry may have been very small. This would tend to obscure a systematic relationship between net entry and rivalry.

Relation of Na+ reabsorption to utilization of O2 and lactate in the perfused rat kidney.

When the ratio delta TNa+/delta QO2 is used to estimate the energy requirements for net Na+ reabsorption (TNa+), it is assumed that the entire change in renal O2 uptake (delta QO2) is utilized only for the delta TNa+. However, if increases in renal synthetic work also occur when TNa+ is increased, the energy cost for TNa+ will be overestimated. We perfused the substrate-limited isolated rat kidney at 38 degrees C, pH 7.4, a mean arterial pressure of 120 mmHg, and mean lactate concentrations between 0 and 8.3 mM. We measured QO2, TNa+, net reabsorption of lactate (Tlac), net utilization of lactate (Qlac), lactate decarboxylation rate (Qlacox), as well as the net entry rate of lactate into biosynthetic pathways (Qxslac). When no exogenous substrate was present (rates are means, g wet wt-1 . min-1) GFR was 351 +/- 38 microliter, %TNa+ was 54 +/- 2%, and QO2 was 2.85 +/- 0.31 mumol; there was also a loss of about 20% of renal tissue K+ content. When mean [lactate] greater than or equal to 0.73 mM, the loss of tissue K+ was completely prevented and %TNa+ increased to and remained at about 85%. At mean [lactate] of 8.3 mM, Tlac was 5.1 +/- 0.6 mumol, QO2 was 6.12 +/- 1.24 mumol, and GFR was 709 +/- 83 microliter. Qlac, delta Qlacox and delta TNa+ increased in parallel with each other and approaches maximal rates as [lactate] was raised. By contrast, Tlac increased as a linear function of perfusate [lactate] and was not related to changes in Qlac. The molar increases in TNa+ were 10- to 20-fold greater than the increases in Tlac. It is more probable, therefore, that lactate enhances TNa+ by providing energy from its oxidation rather than by a co-transport phenomenon. At all concentrations of lactate, more lactate was utilized (Km = 1.2 mM; Vmax = 3.4) than was decarboxylated (Km = 1.6 mM; Vmax = 1.7), indicating that as lactate concentration increased, both the synthesis of new products from lactate and Na+ reabsorption increased. We conclude that the ratio delta TNa+/delta QO2, overestimates the energy cost of Na+ reabsorption. In order to obtain an accurate estimate of the energy requirements for TNa+ in kidney, the simultaneous changes in the rate of net biosynthetic work must also be quantified as TNa+ is changed.

Light-triggered proton movements in retinal discs from the frog

Illumination of retinal discs from dark adapted frogs caused a rapid and transient alkalinization of the suspension medium, followed by a slower and more prolonged acidification. Pretreatment with valinomycin, gramicidin or a proton conductor did not change this pattern, but the initial proton uptake was prevented by concentrations of a detergent or alcohol that had no effect on the acidification process. The initial transient proton uptake corresponded to a minimum of 5.7 H + taken up per rhodopsin bleached, with an elevation of this stoichiometry at early times of illumination. It is suggested that bleaching of rhodopsin contained in retinal discs initiates a transmembrane ion flux that is reflected by a net proton entry.

A Simultaneous Equation Analysis of the Structure and Performance of the United States Petroleum Refining Industry

formulation of the Structure-Conduct-Performance paradigm [I3], [14] has been predominantly concerned with the relationship between industrial concentration and profitability. In fact, it may be one of the most frequently tested relationships in economics. Professor Leonard Weiss compiled a table of 46 concentration-profitability studies for the I974 Columbia Law School Conference on Industrial Concentration and referred to another eight in a footnote [35]. Without exception, these studies specify and estimate single-equation models in which causality runs from structure to performance. The thesis of this paper is that these studies are misspecified-that structure may indeed influence profitability, but that profitability may, in turn, affect capacity expansion and net entry, two determinants of industrial structure. A correct specification of the economic phenomena would be with a set of equations that are necessarily both dynamic and simultaneously related.1 If this more detailed specification of the Mason paradigm is to have any value, however, it must have implications alternative to those accruing from single-equation studies. In this paper a dynamic simultaneous equation model will be specified, and two such implications will be examined. One relates to a possible source of bias in the single-equation results, and the second concerns the impact that changes in exogenous variables may have on endogenous variables. Although there has been debate as to the validity of the findings of the

Kinetics of 3-O-methyl-D-glucose transport in isolated rat hepatocytes.

3-O-Methyl-D-glucose transport across the plasma membrane of isolated rat hepatocytes was followed for net entry of the sugar into sugar-free cells (zero trans entry), net exit of sugar into sugar-free medium (zero trans exit) and for unidirectional entry and exit fluxes when cells had been equilibrated with sugar in the extracellular medium (equilibrium exchange entry and exit). These measurements were performed at 20 degrees C and pH 7.4 by the use of simple manual methods. Initial rates of transport showed a Michaelis--Menten dependency on the sugar concentration at the cis side of the membrane over the range of concentrations tested (100 microM to 100 mM). Transport was found to be symmetrical with no evidence of substrate stimulation of transport from the trans side of the membrane. Parameters (mean values +/- S.E.M.) of transport were estimated as Vmax. 86.2 +/- 9.7 mmol/litre of cell water per min and Km 18.1 +/- 5.9 mM for exchange entry, Vmax. 78.8 +/- 5.3 mmol/litre of cell water per min and Km 17.6 +/- 3.5 mM for exchange exit, Vmax. 84.1 +/- 8.4 mmol/litre of cell water per min and Km 16.8 +/- 4.6 mM for zero trans exit.

TRYPTOPHAN TRANSPORT ACROSS THE BLOOD‐BRAIN BARRIER DURING ACUTE HEPATIC FAILURE

Abstract— Tryptophan transport across the blood‐brain barrier was studied using a single injection dual isotope label technique, in the following three conditions: normal rats, rats with portacaval shunts, and rats with portacaval shunts followed 65 h later by hepatic artery ligation. In both normal rats and those with acute hepatic failure the tryptophan transport system was found to be comprised of two kinetically distinct components. One component was saturable and obeyed Michaelis‐Menten kinetics (normal: Vmax= 19.5 nmol.min−1.g−1. Km= 113 μM; hepatic failure: Vmax, = 33.8 nmol.min−1.g−1, Km= 108 μM), and the second was a high capacity system which transported tryptophan in direct proportion to concentration over the range tested (normal: K= 0.026 ml.min−1.g−1; hepatic failure: K= 0.067 ml.min−1.g−1). Since the saturable low capacity component transports several neutral amino acids, and their collective plasma concentration is high in relation to the individual Kms, tryptophan transport by this component is reduced by competitive inhibition under physiological conditions. Thus it was calculated that in normal rats approx 40% of tryptophan influx occurs via the high capacity system. During acute hepatic failure transport via both components was increased substantially, approximately doubling the rate of tryptophan penetration of the blood‐brain barrier at all concentrations tested. The contribution by the high capacity component became even more significant than in normal rats, accounting for about 75% of all tryptophan passage from plasma to brain. Brain tryptophan content was 29.9 nmol/g in normal rats and rose to 45.2 nmol/g in rats with portacaval shunts and 50.5 nmol/g in those with acute hepatic failure, correlating with the increased rate of tryptophan transport. In a previous study we found that plasma competing amino acids were greatly increased during acute hepatic failure. Calculations predict that these increased concentrations would cause a reduction in tryptophan transport by the low capacity system. However, because of the increase in the rate of transport by the high capacity component, net tryptophan entry across the blood‐brain barrier was actually increased. This increased rate of transport clearly contributes to the increased content of brain tryptophan found during hepatic failure.

Effects of external sodium and cell membrane potential on intracellular chloride activity in gallbladder epithelium.

Conventional and Cl-selective liquid ion-exchanger intracellular microelectrodes were employed to study the effects of extracellular ionic substitutions on intracellular Cl activity (aCli) in Necturus gallbladder epithelium. As shown previously (Reuss, L., Weinman, S.A., 1979; J. Membrane Biol. 49:345), when the tissue was exposed to NaCl-Ringer on both sides aCli was about 30 mM, i.e., much higher than the activity predicted from equilibrium distribution (aCleq) across either membrane (5--9 mM). Removal of Cl from the apical side caused a reversible decrease of aCli towards the equilibrium value across the basolateral membrane. A new steady-state aCli was reached in about 10 min. Removal of Na from the mucosal medium or from both media also caused reversible decreases of aCli when Li, choline, tetramethylammonium or N-methyl-D-glucamine (NMDG) were employed to replace Na. During bilateral Na substitutions with choline the cells depolarized significantly. However, no change of cell potential was observed when NMDG was employed as Na substitute. Na replacements with choline or NMDG on the serosal side only did not change aCli. When K substituted for mucosal Na, the cells depolarized and aCli rose significantly. Combinations of K for Na and Cl for SO4 substitutions showed that net Cl entry during cell depolarization can take place across either membrane. The increase of aCli in depolarized cells exposed to K2SO4-Ringer on the mucosal side indicates that the basolateral membrane Cl permeability (PCl) increased. These results support the hypothesis that NaCl entry at the apical membrane occurs by an electroneutral mechanism, driven by the Na electrochemical gradient. In addition, we suggest that Cl entry during cell depolarization is downhill and involves an increase of basolateral membrane PCl.

Regulation of cell volume in separated renal tubules incubated in hypotonic medium

The regulation of cell volume was studied in separated renal tubules (SRT) whose basement membrane had been removed by collagenase. Regulation occurred when SRT were immersed in a hypotonic medium, the increase in cellular water content being half that expected in the absence of regulation. Regulation was immediate, with no initial swelling, and was accompanied by a loss of NaCl, with no change in cellular K. This regulation was eliminated by 10(-3) M ouabain. We conclude that: 1) Cell volume regulation which occurs in a hypotonic medium is due to an immediate loss of NaCl. 2) Loss of NaCl might be due to blocking of the net passive NaCl entry into the cells resulting from the drop in the transmembrane NaCl electrochemical gradient. The high membrane sodium permeability, probably located on the luminal side of the tubular cells, might explain why regulation was instantaneous. 3) Elimination of volume regulation by ouabain suggests there is no need to assume that a ouabain-insensitive pump regulates cell volume.

Movements of monosaccharides between blood and tissues of vascularly perfused small intestine.

1. A method involving the analysis of pulse transients of the vascular concentrations of test sugar and extracellular marker has been used to study the movements of non-metabolized sugars between the cells and vascular fluid of the vascularly perfused small intestine of R. ridibunda. Reasons are given for supposing that the method does properly measure the net entry of sugars into a cellular compartment that includes at least the epithelium. 2. It is found that while the glucose analogues, 3-O-methyl-D-glucose (3MG) and 2-deoxy-D-glucose (2)DG) are able to enter a cellular compartment when they are added to the vascular bed, alpha-methyl-D-glucoside (alpha MG) is able to enter the compartment only at a very slow rate from the vascular bed. In contrast, 3MG and alaph MG are well absorbed from the lumen whereas the inward permeability of 2DG across the lumen face of the epithelium is very low and, unlike 3MG and alpha MG, is not influenced by the presence in the lumen of other transported sugars. 3. The presence of phlorizin in the intestinal lumen increases the flux of alpha MG and of 3MG in the direction vascular bed--bulk phase of lumen. Reasons are given for supposing that the movement of sugars from the vascular bed into the lumen may involve a cellular route but occurs, at least in part, through a paracellular, extracellular route. 4. The exit of monosaccharides that have been loaded previously into the epithelium either from the lumen or from the vascular bed has been investigated. 3MG washes out rapidly into the vascular bed and the exit is stimulated by the addition of D-glucose to the intestinal lumen and by the addition of 2DG, but not alpha MG, to the arterial infusate. In contrast, alpha MG, loaded into the epithelium from the lumen, washes out of the cells only slowly into the vascular bed, so that even with high rates of vascular perfusion alpha MG accumulates within the tissue. The sustained accumulation of alpha MG implies that not only is the permeability for exit into the blood restricted for this sugar, but also the permeability is low across the brush border in an outward direction, cell to lumen ('lobster pot effect'). The wash-out of 3MG into the vascular effluent is sufficently rapid that only in the absence of vascular perfusion is 3MG accumulated within the tissue. 5. The contrasting properties of the monosaccharide transport systems accessible from the intestinal lumen and the vascular bed respectively are discussed in relation to the problems of epithelial transport of monosaccharide.

Calcium entry leads to inactivation of calcium channel in Paramecium.

Under depolarizing voltage clamp of Paramecium an inward calcium current developed and subsequently relaxed within 10 milliseconds. The relaxation was substantially slowed when most of the extracellular calcium was replaced by either strontium or barium. Evidence is presented that the relaxation is not accounted for by a drop in electromotive force acting on calcium, or by activation of a delayed potassium current. Relaxation of the current must, therefore, result from an inactivation of the calcium channel. This inactivation persisted after a pulse, as manifested by a reduced calcium current during subsequent depolarization. Inactivation was retarded by procedures that reduce net entry of calcium, and was independent of membrane potential. The calcium channel undergoes inactivation as a consequence of calcium entry during depolarization. In this respect, inactivation of the calcium channel departs qualitatively from the behavior described in the Hodgkin-Huxley model of the sodium channel.

Glucose lactate interrelations in sheep.

The constant-infusion, isotope-dilution method was used to investigate the interrelationships between the glucose and lactate pools of six trained sheep deprived of food overnight. Arterial plasma lactate concentration was a linear function of the net lactate entry rate as was the net production of glucose from lactate, which suggests that the net rate of formation of glucose from lactate is dependent on the availability of lactate. Similarly the arterial plasma glucose concentration was correlated with the net entry rate of glucose as was the net production rate of lactate from glucose, suggesting that the net rate of lactate production from glucose is a function of arterial plasma glucose concentration. The demonstration of these two interrelations between glucose and lactate in normal sheep suggests that, in the absence of external factors producing hormonal or other changes that could cause perturbations of carbohydrate homeostasis, the net rates of conversion of glucose to lactate and of lactate to glucose may be largely determined by the arterial concentrations of glucose and lactate, respectively.

Properties of the calcium‐extruding mechanism of liver cells.

1. The movements of Ca2+ between liver slices and the suspending medium have been followed with a Ca2+-specific electrode and with measurements of the efflux of 45Ca. 2. A net entry of Ca2+ into the tissue occurred during anaerobiosis. Reoxygenation of the medium resulted in a net extrusion of Ca2+ which was reversed by the addition of a respiratory inhibitor (Amytal), an uncoupler of oxidative phosphorylation (pentachlorophenol) or the divalent-cation-specific ionophore, A23187. 3. The net extrusion of Ca2+ was dependent on the presence of Mg2+ in the medium, but was not prevented by ouabain or by incubation in a Na+-free medium. Extrusion was not prevented by cytochalasin B or colchicine. 4. The undirectional efflux of 45Ca required Mg2+ to attain its maximal rate, and the magnitude was not affected by the presence of ouabain or the absence of Na+ from the medium. 5. It is concluded that extrusion of Ca2+ from liver cells is a metabolically dependent transport process that occurs independently of the exchange of Na+ between tissue and medium.

An efflux mechanism determines the low net entry of lithium in yeasts

Lithium is a toxic cation for yeasts and many strains keep a lower concentration in the cytoplasm than that present in the medium [l] . A transmembrane electrical potential, negative inside, is in increasing evidence in yeasts [2-51, similar to that found in Neurospora [6] and also in bacteria, where it draws K’ into the cell [7]. This potential would draw any cation into the cytoplasm, provided the appropriate channel exists and it is known that Li’ enters into the yeast cell through the K’ carrier [8] which seems to be dissociated from the energy coupling [4]. So the maintenance of a lower Li’ concentration in the cytoplasm than in the medium would require a system to exclude this cation. In this paper we present kinetic evidence for such a system.

Amino acid transport systems in animal cells: interrelations and energization.

AbstractAfter summarizing the discrimination of the several transport systems of neutral amino acids in the cell of the higher animal, I discuss here the ways in which 2 dissimilar transport systems interact, so that one tends to run forward for net entry and the other backwards for net exodus. An evaluation of the proposals for energization shows that uphill transport continues when neither alkali‐ion gradients nor ATP levels are favorable. Evidence is presented that under these conditions a major contribution is made by another mode of energization, which may depend on the fueling of an oxidoreductase in the plasma membrane. This fueling may involve the export by the mitochondrion of the reducing equivalents of NADH by one of the known shuttles, e.g., the malate‐aspartate shuttle. After depletion of the energy reseves in the Ehrilich cell by treating it with dinitrophenol plus iodoacetate concentrative uptake of test amino acids is restoration by pyruvate but in poor correlation with the restoration of alkali‐ion gradients and ATP levels. This restoration by pyruvate but not by glucose is highly senstitive to rotenone. A combination of phenazine methosulfate and ascorbate will also produce transport restoration, before either the alkali‐ion gradients or ATP levels have begun to rise. The restoration of transport applies to a model amino acid entering by the Na+‐independent system, as well as to one entering by the principal Na+‐dependent system, restoration being blocked by ouabain, despite the weak effect of ouabain on the alkali‐ion gradients in the Ehrlich cell. Quinacrine terminates very quickly the uptake of model amino acids, before the alkali‐ion gradients have begun to fall and before the ATP level has been halved. Quinacrine is also effective in blocking restoration of uphill transport by either pyruvate or the phenazine reagent. Preliminary results show that vesicles prepared from the plasma membrane of the Ehrlich cell quickly reduce cytochrome c or ferricyanide in the presence of NADH, and that the distribution of a test amino acid between the vesicle and its environment is influenced by NADH, quinacrine, and an uncoupling agent in ways consistent with the above proposal, assuming that a majority of the vesicles are everted.

Changes in membrane currents in bullfrog atrium produced by acetylcholine.

1. A double sucrose-gap voltage-clamp technique has been used to study the effects of acetylcholine on the membrane currents in atrial trabeculae of the bullfrog, Rana catesbeiana. 2. The second, or slow inward (Ca2+/Na+) current, was found to be markedly reduced by concentrations of acetylcholine greater than approximately 2-0 X 10(-8)M. The resulting decrease in net calcium entry provides a straightforward explanation for the negative inotropic action of acetylcholine in atrial muscle. 3. Measurements of membrane resistance near the resting potential showed that relatively high doses of acetylcholine (approximately 10(-7) M) decrease membrane resistance by about twofold. This effect is shown to be the result of an increase in a time-independent background current which appears to be carried mainly by potassium ions. 4. Using appropriate pharmacological techniques, it has been possible to demonstrate: (i) that the peak slow inward current is reduced to about half its initial value before any significant increase in background current occurs; (ii) that even when a sufficient dose of acetylcholine to produce an increase in background current is used, the background current shows inward-going rectification and cannot account for the observed reduction in the slow inward current. 5. No consistent change was observed in the degree of activation of the time-dependent outward membrane currents after application of concentrations of acetylcholine which produced large decreases in the peak slow inward current. 6. These results are discussed in relation to previous electro-physiological and radioisotope studies of the mechanism of the negative inotropic effect of acetylcholine in cardiac muscle.

Phosphate, calcium and magnesium fluxes into the lumen of the rat proximal convoluted tubule.

In order to study fluxes of phosphate (Pi), Ca and Mg into the rat proximal tubule, a modification of the split-droplet microinjection technique was used. Injected fluids were isotonic solutions containing no Pi, Ca or Mg. The initial NaCl concentration of the injectates was either (a) 115 mM(l (which resulted in net fluid entry into the lumen), (b) 125 mM/l (no net fluid movement) or (c) 150 mM/l (net reabsorption of fluid). Injected droplets were subsequently collected from the nephron and their ionic concentrations determined using electron probe analysis. All 3 ions entered the tubular lumen. For the 115 mM and 125 mM NaCl injectates, Pi concentration increased for the first 15 s, then reached steady values of 2.07 mM/l and 2.30 mM/l respectively. Using 150 mM NaCl as injectate, Pi concentration increased for only 10 s, and then reached an average value of 2.04 mM/l. Ca and Mg concentrations in reaspirated droplets showed no correlation with time, indicating that entry into the lumen was almost immediate. The mean Ca concentration using 115 mM NaCl injectate was 1.63 mM/l, higher than with equilibrated or reabsorbed injectates (1.01 and 1.15 mM/l respectively). Mg concentration following injection of 115 mM NaCl solution (0.45 mM/l) was lower than with the other 2 injectates (0.92 and 0.85 mM/l). It is suggested that Pi and Mg enter the proximal tubular lumen from the tubular cells, while Ca entry may be transtubular and take place via intercellular pathways.

The control of anaerobic glycolysis by glucose transport and ouabain in slices of hepatoma 3924A

1. 1. The activities of glycolysis and K + transport have been studied in slices of Morris hepatoma 3924A incubated under anaerobic conditions in the presence of different concentrations of glucose (1–50 mM). 2. 2. Ouabain-sensitive net transport of K + was observed at all glucose concentrations greater than 1 mM; ouabain reduced the rate of glycolysis by about 25% at all glucose concentrations able to support ion transport. 3. 3. The net entry of glucose into the intracellular phase was studied at varying glucose concentrations. The rate of glucose entry was similar to the rate of glucose utilisation by anaerobic glucolysis at medium concentrations of 10 mM and less, but exceeded the rate of glycolysis at 20 mM and above. 4. 4. The glucose entry was not Na +-dependent and was not inhibited by ouabain. 5. 5. The results suggest (a) that the reduction in glucolytic activity caused by ouabain is not due to an inhibition of glucose transport and (b) that the glucose transport system of this poorly differentiated hepatoma has properties similar to that of normal liver.

Concanavalin A-induced alterations in sodium and potassium content of Ehrlich ascites tumor cells.

AbstractNet fluxes of sodium and potassium were studied in Ehrlich mouse ascites tumor cells during contact with the agglutinating protein, concanavalin A. This lectin altered cation transport markedly at concentrations of 20–105 μg/ml (6–47 μg/mg cell protein). Whereas control cells extruded sodium and maintained or accumulated potassium against electrochemical gradients, in the presence of concanavalin A there was rapid net sodium entry and potassium loss. After 10–20 minutes in concanavalin A, sodium extrusion began and potassium loss diminished but these events were prevented by ouabain. The alterations in cation content induced by concanavalin A are unlikely to be the result only of agglutination since soybean agglutinin caused much smaller changes although it agglutinated the cells equally well.

Influence of chloride ions on changes in membrane potential during prolonged application of carbachol to frog skeletal muscle.

1. Micro-electrodes were used to follow changes in the membrane potential at the end-plate region of single fibres in narrow strips of frog skeletal muscle exposed to carbachol applied in continuously flowing Ringer solution containing tetrodotoxin (200 nM) and neostigmine (3 muM).2. The depolarizations elicited by carbachol (5-20 muM) usually developed in two phases, the first of which was generally complete within 30 s whereas several min were required for the second.3. Repolarization after carbachol also occurred in two phases, the second of which outlasted the time needed to clear the bath, and varied with the magnitude and duration of the depolarization which carbachol had caused.4. These findings could best be explained in terms of the consequences of net entry of chloride ions into the fibre during the depolarization caused by carbachol. This hypothesis is supported by three lines of evidence:(a) Replacement of the chloride content of the Ringer solution by the less permeant anion isethionate abolished the slow phases of the carbachol response.(b) Reduction of chloride permeability (by lowering pH) caused rapid repolarization during the recovery period after carbachol.(c) When the membrane potential was clamped at the resting level throughout the action of carbachol, so avoiding chloride redistribution, the clamping current records did not show the slow phases attributed to chloride movement.5. Chloride redistribution contributes to the gradual spread of depolarization during prolonged applications of depolarizing agents to skeletal muscle. It also complicates the interpretation of the dose-response relationship, and may make it more difficult to assess the extent to which the receptors become desensitized during the action of agonists applied in the bath.

Entry, Concentration Change, and Stability of Market Shares

Traditional theory assigns entry (exit) a prominent role. Yet, there have been relatively few attempts to ascertain, empirically, the effects of actual entry rates.' In particular, we lack good information on the impacts of entry on the structure and performance of industries. This paper considers the impacts of entry on two commonly employed measures of market structure. Specifically, I investigate the relationship between actual rates of net entry, and concentration change and market share stability.