Biomedical subjects

Young C Kim

Publications and source records attributed to Young C Kim.

At least 19 recordsLinked to original sources

PubMed2026

Molecular origins of pH gradients in charge-regulated biomolecular condensates.

Biomolecular condensates exhibit spontaneous electrochemical microenvironments characterized by asymmetric ion distributions and pH gradients that emerge from protein-sequence-dependent charge regulation. Despite their biological importance, mechanistic understanding of these microenvironments has been constrained by the absence of computationally tractable frameworks capable of treating proton exchange, counterion partitioning, and buffer equilibria on consistent thermodynamic footing. Here, we introduce the buffered Charge-Regulation Monte Carlo (b-CR-MC) framework, which couples grand-canonical exchange of ions and buffer species with explicit charge regulation of titratable residues. By extending the CR-MC ion-merging strategy to multicomponent reservoirs and employing the restricted primitive model, b-CR-MC achieves computational efficiency while maintaining thermodynamic rigor, achievingquantitative agreement with the more expensive generalized grand-reaction Monte Carlo approach. Applied to full-length FUS (net positive) and PGL-3 (net negative) under physiological conditions, the framework reveals sequence-dependent pH gradients: the dense phase of FUS exhibits an alkaline shift, while that of PGL-3 exhibits an acidic shift, in both cases driving the condensate interior toward the protein's isoelectric point. Slab-geometry simulations further resolve the Donnan potential and continuous ion profiles across the condensate interface, confirming the direction of these electrochemical shifts. Additionally, we identify spatially resolved buffer depletion within dense phases, establishing that dynamic charge regulation is a primary determinant rather than a secondary correction to condensate electrochemistry. By establishing a sequence-resolved, thermodynamically consistent computational platform, b-CR-MC enables quantitative prediction of how mutations and post-translational modifications reprogram condensate microenvironments across biological and pathophysiological contexts.

Hydrogen-Ion Concentration↗

PubMed2007

Mitochondrial isocitrate dehydrogenase protects human neuroblastoma SH-SY5Y cells against oxidative stress.

The neuroprotective effect of mitochondrial isocitrate dehydrogenase (IDPm), an enzyme involved in the reduction of NADP(+) to NADPH and the supply of glutathione (GSH) in mitochondria, was examined using SH-SY5Y cells overexpressing IDPm (S1). S1 cells showed higher NADPH and GSH levels than vector transfectant (V) cells and were more resistant to staurosporine-induced cell death than controls. Staurosporine-induced cytochrome c release, caspase-3 activation, and production of reactive oxygen species (ROS) were significantly attenuated in S1 cells as compared to V cells and reduced by antioxidants, trolox and GSH-ethyl ester (GSH-EE). Staurosporine-induced the release of Mcl-1 from mitochondria that formed a complex with Bim. Mcl-1 was then cleaved to a shortened form in a caspase-3 dependent manner; its release was attenuated far more in S1 than in V cells after staurosporine treatment. Finally, the staurosporine-induced decrease in mitochondrial membrane potential (Deltapsi(m)) was correlated with the time of mitochondrial Mcl-1 release; the loss of Deltapsi(m) was attenuated significantly in S1 cells as compared to that in V cells. These results suggest that the neuroprotective effect of IDPm may result from increases in NADPH and GSH levels in the mitochondria. This, in turn, inhibits mitochondrial ROS production after cytochrome c release, which seems to be mediated through Mcl-1 release.

Antioxidants↗

PubMed2006

Contrasting changes in phase I and phase II metabolism of acetaminophen in male mice pretreated with carbon tetrachloride.

Effect of carbon tetrachloride (CCl(4)) pretreatment on the biotransformation and elimination of acetaminophen were examined in male mice. A 24 hr initial dose of CCl(4) (0.05 ml/kg, intraperitioneally) reduced the induction of hepatotoxicity resulting from acetaminophen treatment (350 mg/kg, intraperitoneally) as determined by changes in serum alanine and aspartate aminotransferase, and sorbitol dehydrogenase activities. Acetaminophen and the major metabolites in plasma were monitored for 12 hr following acetaminophen treatment. CCl(4) pretreatment decreased the plasma concentrations of acetaminophen-cysteine and acetaminophen-mercapturate, but acetaminophen-glucuronide and acetaminophen-sulfate were increased significantly. The elimination of the parent drug from plasma was not affected by CCl(4). In urine collected for 24 hr, the concentrations of acetaminophen-sulfate and acetaminophen-glucuronide were increased by 84% and 33%, respectively, whilst acetaminophen-cysteine and acetaminophen-mercapturate were reduced to approximately one third of control. Expression of cytochrome P450 (CYP) isozymes was determined using antibodies of 2E1 and 1A2 as probes. CYP2E1 and 1A2 expressions were decreased significantly by CCl(4). Likewise, CCl(4) treatment reduced the microsomal p-nitrophenol hydroxylase and p-nitroanisole O-demethylase activities to less than one third of control. The results indicate that, although CCl(4) reduces the generation of thioether conjugates of acetaminophen by decreasing the CYP activities, inhibition of the oxidative metabolism of acetaminophen is counterbalanced by the enhancement of conjugate formation via the glucuronide and sulfate pathways, resulting in elimination of the drug at a rate equivalent to that in normal mice. It is suggested that liver injury in patients may not warrant a mandatory reduction of drug doses extensively inactivated via phase II reactions.

Acetaminophen↗

PubMed2005

Universality of ionic criticality: size- and charge-asymmetric electrolytes.

Grand-canonical simulations designed to resolve critical universality classes are reported for z:1 hard-core electrolyte models with diameter ratios lambda=a+/a- less than or approximately equal 6. For z=1 Ising-type behavior prevails. Unbiased estimates of Tc(lambda) are within 1% of previous (biased) estimates but the critical densities are approximately 5% lower. Ising character is also established for the 2:1 and 3:1 equisized models, along with critical amplitudes and improved Tc estimates. For z=3, however, strong finite-size effects reduce the confidence level although classical and O (n>or=3) criticality are excluded.

Journal Article↗

PubMed2005

Kinesin crouches to sprint but resists pushing.

Recent optical trap experiments have applied resisting, assisting, and sideways loads to conventional kinesin moving on microtubules at fixed [ATP]. To gain insight into intermediate motions when the motor protein takes its 8.2-nm steps, the velocity and randomness data have been analyzed by using discrete-state stochastic models with a three-dimensional "energy landscape." The bead size and tether angle play a crucial role. The analysis implies that on binding ATP the motor "crouches," the point of attachment of the tether at the necklinker junction moving downward toward the microtubule by 0.5-0.7 nm, while inching forward by only 0.1-0.2 nm, before completing the step from a transition state by a unitary "sprint" of approximately 7.8 nm. These inferences accord with high-resolution observations that exclude a previously predicted substep of 1.8-2.1 nm. Assisting and leftward loads are opposed in that the perpendicular component of the tension in the tether is enhanced by approximately 2 pN, which reduces the velocity, but sideways lurching is not supported.

Adenosine Triphosphate↗

PubMed2005

Screening in ionic systems: simulations for the Lebowitz length.

Simulations of the Lebowitz length, xiL (T, rho), are reported for the restricted primitive model hard-core (diameter a) 1:1 electrolyte for densities rho approximately < 4rho(c) and T(c) approximately < T approximately < 40T(c). Finite-size effects are elucidated for the charge fluctuations in various subdomains that serve to evaluate xiL. On extrapolation to the bulk limit for T approximately > 10T(c) the exact low-density expansions are seen to fail badly when rho > 1/10 rho(c) (with rho(c)a3 approximately = 0.08). At higher densities xiL rises above the Debye length, xiD proportional to square root(T/rho), by 10%-30% (up to rho approximately =1.3rho(c)); the variation is portrayed fairly well by the generalized Debye-Hückel theory. On approaching criticality at fixed rho or fixed T, xiL (T, rho) remains finite with xiL(c) approximately = 0.30a approximately = 1.3xiD(c) but displays a weak entropylike singularity.

Journal Article↗

PubMed2005

Yang-Yang anomalies and coexistence diameters: simulation of asymmetric fluids.

A general method for estimating the Yang-Yang ratio, R(mu) , of a model fluid via Monte Carlo simulations is presented on the basis of data for a hard-core square-well (HCSW) fluid and the restricted primitive model (RPM) electrolyte. The isothermal minima of Q(L)(triple bond) 2L/ L scaling are evaluated at T(c) in an LxLxL box where m=rho- L is the density fluctuation. The "complete" finite-size scaling theory for the Q(+/-)(min) (T(c);L) incorporates pressure mixing in the scaling fields, thereby allowing for a Yang-Yang anomaly. It yields a dominant term in the asymmetry, Q(+)(min)-Q(-)(min) , varying as L(-beta/nu) with an amplitude proportional to the crucial pressure-mixing coefficient, j(2) . The reliably known critical order-parameter distribution for (d=3) Ising systems then enables one to estimate j(2) , thereby yielding R(mu) , from the Q minima together with information on the nonuniversal amplitudes for the order parameter and the susceptibility. The detailed analysis needed to estimate j(2) for an HCSW fluid and the RPM is presented. Furthermore, the Q-minima below T(c) can also provide the coexistence-curve diameters, rho(diam) (T) (triple bond)1/2 (rho(+) + rho(-)) , very close to T(c) for both models: here rho +/-(T) are the densities of the coexisting liquid and gas phases. The recently developed recursive scaling algorithm for Deltarho(infinity) (T) (triple bond)rho(+)-rho(-) is adapted to investigate the corresponding universal scaling functions. The two extremal forms of these scaling functions are computed with the aid of the exactly soluble decorated lattice-gas model. The critical densities for the RPM and HCSW fluid found via this route are consistent with previous estimates obtained from the data above T(c) ; the magnitudes of the |T- T(c)|(2beta) and |T- T(c)|(1-alpha) corrections to rho(diam)(T) are estimated.

Journal Article↗

PubMed2005

Convergence of fine-lattice discretization for near-critical fluids.

In simulating continuum model fluids that undergo phase separation and criticality, significant gains in computational efficiency may be had by confining the particles to the sites of a lattice of sufficiently fine spacing, a(0) (relative to the particle size, say a). But a cardinal question, investigated here, then arises; namely, How does the choice of the lattice discretization parameter, zeta identical with a/a(0), affect the values of interesting parameters, specifically, critical temperature and density, T(c) and rho(c)? Indeed, for small zeta ( less, similar 4-8) the underlying lattice can strongly influence the thermodynamic properties. A heuristic argument, essentially exact in d = 1 and d = 2 dimensions, indicates that, for models with hard-core potentials, both T(c)(zeta) and rho(c)(zeta) should converge to their continuum limits as 1/zeta((d)(+1)/2) for d </= 3 when zeta --> infinity; but the behavior of the error is highly erratic for d >/= 2. For smoother interaction potentials, the convergence is faster. Exact results for d = 1 models of van der Waals character confirm this; however, an optimal choice of zeta can improve the rate of convergence by a factor 1/zeta. For d >/= 2 models, the convergence of the second virial coefficients to their continuum limits likewise exhibits erratic behavior, which is seen to transfer similarly to T(c) and rho(c); but this can be used in various ways to enhance convergence and improve extrapolation to zeta = infinity as is illustrated using data for the restricted primitive model electrolyte.

Journal Article↗

PubMed2005

Effects of betaine supplementation on hepatic metabolism of sulfur-containing amino acids in mice.

BACKGROUND/AIMS: We previously reported that acute betaine treatment induced significant changes in the hepatic glutathione and cysteine levels in mice and rats. The present study was aimed to determine the effects of dietary betaine on the metabolism of sulfur-containing amino acids. METHODS/RESULTS: Male mice were supplemented with betaine (1%) in drinking water for up to 3 weeks. Changes in hepatic levels of major sulfur amino acid metabolites and products were stabilized after 2 weeks of betaine supplementation. Betaine intake increased methionine, S-adenosylmethionine, and S-adenosylhomocysteine levels significantly, but homocysteine and cystathionine were reduced. Methionine adenosyltransferase activity was elevated to three-fold of control. Cysteine catabolism to taurine was inhibited as evidenced by a decrease in cysteine dioxygenase activity and taurine levels in liver and plasma. Despite the significant changes in the transsulfuration reactions, neither hepatic cysteine nor glutathione was altered. Betaine supplementation decreased the hepatotoxicity induced by chloroform (0.5 ml/kg, ip) significantly. CONCLUSIONS: Betaine supplementation enhances recycling of homocysteine for the generation of methionine and S-adenosylmethionine while reducing its utilization for the synthesis of cystathionine and cysteine. However, the hepatic levels of cysteine or glutathione are not affected, most probably due to the depression of taurine generation from cysteine.

Amino Acids, Sulfur↗

PubMed2005

Effect of betaine supplementation on changes in hepatic metabolism of sulfur-containing amino acids and experimental cholestasis induced by alpha-naphthylisothiocyanate.

Alterations in the hepatic metabolism of sulfur amino acids in experimental cholestasis induced by alpha-naphthylisothiocyanate (ANIT) (100 mg/kg, po) were monitored in male mice for 1 week. We also examined the effects of betaine supplementation (1% in drinking water) for 2 weeks on the hepatotoxicity and changes in the sulfur amino acid metabolism induced by ANIT treatment. Acute ANIT challenge elevated the serum alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST) activities, and total bilirubin contents from 5 h after the treatment, reaching a peak at t = 48-72 h. Hepatic S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) levels were decreased significantly in a manner almost inversely proportional to the changes in serum parameters measured to determine the ANIT-induced toxicity. Hepatic glutathione and cysteine levels were elevated at t = 120 h after the treatment. Betaine supplementation blocked or significantly attenuated induction of the hepatotoxicity by ANIT. The decrease in SAM and SAH levels was also inhibited by betaine intake. The results indicate that betaine supplementation may antagonize the induction of experimental cholestasis and changes in the metabolism of sulfur amino acids associated with ANIT treatment. The underlying mechanism and pharmacological significance of its action are discussed.

1-Naphthylisothiocyanate↗

PubMed2004

Discretization dependence of criticality in model fluids: a hard-core electrolyte.

Grand-canonical simulations at various levels, zeta=5-20, of fine-lattice discretization are reported for the near-critical 1:1 hard-core electrolyte or restricted primitive model (RPM). With the aid of finite-size scaling analyses, it is shown convincingly that, contrary to recent suggestions, the universal critical behavior is independent of zeta (> or approximately 4), thus the continuum (zeta--> infinity ) RPM exhibits Ising-type (as against classical, self-avoiding walk, XY, etc.) criticality. A general consideration of lattice discretization provides effective extrapolation of the intrinsically erratic zeta dependence, yielding (T*(c),rho*(c)) approximately equal to (0.0493(3),0.075) for the zeta=infinity RPM.

Journal Article↗

PubMed2004

Systemic administration of 17beta-estradiol reduces apoptotic cell death and improves functional recovery following traumatic spinal cord injury in rats.

Recent evidence indicates that estrogen exerts neuroprotective effects in both brain injury and neurodegenerative diseases. We examined the protective effect of estrogen on functional recovery after spinal cord injury (SCI) in rats. 17beta-estradiol (3, 100, or 300 microg/kg) was administered intravenously 1-2 h prior to injury (pre-treatment), and animals were then subjected to a mild, weight-drop spinal cord contusion injury. Estradiol treatment significantly improved hind limb motor function as determined by the Basso-Beattie-Bresnahan (BBB) locomotor open field behavioral rating test. Fifteen to 30 days after SCI, BBB scores were significantly higher in estradiol-treated (100 microg/kg) rats when compared to vehicle-treated rats. Morphological analysis showed that lesion sizes increased progressively in either vehicle-treated or 17beta-estradiol-treated spinal cords. However, in response to treatment with 17beta-estradiol, the lesion size was significantly reduced 18-28 days after SCI when compared to vehicle-treated controls. Terminal deoxynucleotidyl transferase-mediated UTP nickend labeling (TUNEL) staining and DNA gel electrophoresis revealed that apoptotic cell death peaked 24-48 h after injury. Also, SCI induced a marked increase in activated caspase-3 in the spinal cord, evident by 4 h after injury. However, administration of 17beta-estradiol significantly reduced the SCI-induced increase in apoptotic cell death and caspase-3 activity after SCI. Furthermore, 17beta-estradiol significantly increased expression of the anti-apoptotic genes, bcl-2 and bcl-x, after SCI while expression of the pro-apoptotic genes, bad and bax, was not affected by drug treatment. Finally, intravenous administration of 17beta-estradiol (100 microg/kg) immediately after injury (post-treatment) also significantly improved hind limb motor function 19-30 days after SCI compared to vehicle-treated controls. These data suggest that after SCI, 17 beta-estradiol treatment improved functional recovery in the injured rat, in part, by reducing apoptotic cell death.

Animals↗

PubMed2004

Manganese superoxide dismutase induced by TNF-beta is regulated transcriptionally by NF-kappaB after spinal cord injury in rats.

Antioxidant enzymes including superoxide dismutase (SOD) may play a role in the mechanism by which cells counteract the deleterious effects of reactive oxygen species (ROS) after spinal cord injury (SCI). Cu/Zn and MnSOD are especially potent scavengers of superoxide anion and likely serve important cytoprotective roles against cellular damage. We investigated expression of SOD after SCI to address its role during the early stages of injury. MnSOD activity was increased 4 h after SCI and persisted at elevated levels up to 24-48 h; by contrast, Cu/ZnSOD activity was not changed. RT-PCR and Western blot analyses showed increased levels of MnSOD mRNA and protein, respectively, by 4 h and reached maximum levels by 24-48 h. Double immunostaining revealed that MnSOD protein was localized within neurons and oligodendrocytes. Tumor necrosis factor-alpha (TNF-alpha) was administered locally into uninjured spinal cords to examine potential mechanisms for MnSOD induction after injury. TNF-alpha administered exogenously increased MnSOD expression in uninjured spinal cords. Western blot and immunostaining also revealed that a transcription factor, NF-kappaB, was activated and translocated into the nuclei of neurons and oligodendrocytes. By contrast, administration of neutralizing antibody against TNF-alpha into injured spinal cords attenuated the increase in MnSOD expression and activation of NF-kappaB. Double immunostaining revealed that MnSOD was co-localized with NF-kappaB in neurons and oligodendrocytes after SCI. These results suggest that TNF-alpha may be an inducer of NF-kappaB activation and MnSOD expression after SCI and that MnSOD expression induced by TNF-alpha is likely mediated through activation of NF-kappaB.

Animals↗

PubMed2004

Minocycline inhibits apoptotic cell death via attenuation of TNF-alpha expression following iNOS/NO induction by lipopolysaccharide in neuron/glia co-cultures.

We attempted to ascertain the neuroprotective effects and mechanisms of minocycline in inflammatory-mediated neurotoxicity using primary neuron/glia co-cultures treated with lipopolysaccharide (LPS). Neuronal cell death was induced by treatment with LPS for 48 h, and the cell damage was assessed using lactate dehydrogenase (LDH) assays and by counting microtubule-associated protein-2 (MAP-2) positive cells. Through terminal transferase deoxyuridine triphosphate-biotin nick end labeling (TUNEL)-staining and by measuring caspase-3 activity, we found that LPS-induced neuronal cell death was mediated by apoptosis. We determined that pre-treatment with minocycline significantly inhibited LPS-induced neuronal cell death. In addition, LPS induced inducible nitric oxide synthase (iNOS) expression significantly, resulting in nitric oxide (NO) production within glial cells, but not in neurons. Both nitric oxide synthase (NOS) inhibitors (N(G)-monomethyl-L-arginine monoacetate (L-NMMA) and S-methylisothiourea sulfate (SMT)) and minocycline inhibited iNOS expression and NO release, and increased neuronal survival in neuron/glia co-cultures. Pre-treatment with minocycline significantly inhibited the rapid and extensive production of tumor necrosis factor-alpha (TNF-alpha) mediated by LPS in glial cells. We also determined that the signaling cascade of LPS-mediated iNOS induction and NO production was mediated by TNF-alpha by using neutralizing antibodies to TNF-alpha. Consequently, our results show that the neuroprotective effect of minocycline is associated with inhibition of iNOS induction and NO production in glial cells, which is mediated by the LPS-induced production of TNF-alpha.

Animals↗

PubMed2003

Effect of age increase on metabolism and toxicity of ethanol in female rats.

Age-dependent change in the effects of acute ethanol administration on female rat liver was investigated. Female Sprague-Dawley rats, each aged 4, 12, or 50 weeks, received ethanol (2 g/kg) via a catheter inserted into a jugular vein. Ethanol elimination rate (EER), most rapid in the 4 weeks old rats, was decreased as the age advanced. Hepatic alcohol dehydrogenase activity was not altered by age, but microsomal p-nitrophenol hydroxylase activity was significantly greater in the 4 weeks old rats. Relative liver weight decreased with age increase in proportion to reduction of EER. Hepatic triglyceride and malondialdehyde concentrations increased spontaneously in the 50 weeks old nai;ve rats. Ethanol administration (3 g/kg, ip) elevated malondialdehyde and triglyceride contents only in the 4 and the 12 weeks old rats. Hepatic glutathione concentration was increasingly reduced by ethanol with age increase. Ethanol decreased cysteine concentration in the 4 weeks old rats, but elevated it significantly in the older rats. Inhibition of gamma-glutamylcysteine synthetase activity by ethanol was greater with age increase, which appeared to be responsible for the increase in hepatic cysteine. The results indicate that age does not affect the ethanol metabolizing capacity of female rat liver, but the overall ethanol metabolism is decreased in accordance with the reduction of relative liver size. Accordingly induction of acute alcoholic fatty liver is less significant in the old rats. However, progressively greater depletion of glutathione by ethanol in older rats suggests that susceptibility of liver to oxidative damage would be increased as animals grow old.

Aging↗

PubMed2003

Asymmetric fluid criticality. II. Finite-size scaling for simulations.

The vapor-liquid critical behavior of intrinsically asymmetric fluids is studied in finite systems of linear dimensions L focusing on periodic boundary conditions, as appropriate for simulations. The recently propounded "complete" thermodynamic (L--> infinity) scaling theory incorporating pressure mixing in the scaling fields as well as corrections to scaling [Phys. Rev. E 67, 061506 (2003)] is extended to finite L, initially in a grand canonical representation. The theory allows for a Yang-Yang anomaly in which, when L--> infinity, the second temperature derivative (d2musigma/dT2) of the chemical potential along the phase boundary musigmaT diverges when T-->Tc-. The finite-size behavior of various special critical loci in the temperature-density or (T,rho) plane, in particular, the k-inflection susceptibility loci and the Q-maximal loci--derived from QL(T, L) is identical with 2L/ L where m is identical with rho- L--is carefully elucidated and shown to be of value in estimating Tc and rhoc. Concrete illustrations are presented for the hard-core square-well fluid and for the restricted primitive model electrolyte including an estimate of the correlation exponent nu that confirms Ising-type character. The treatment is extended to the canonical representation where further complications appear.

Computer Simulation↗

PubMed2003

Precise simulation of near-critical fluid coexistence.

We present a novel method to derive liquid-gas coexisting densities, rho(+/-)(T), from grand canonical simulations (without knowledge of T(c) or criticality class). The minima of Q(L) identical with (2)(L)/ (L) in an LxLxL box with m=rho- (L) are used to generate recursively an unbiased universal finite-size scaling function. Monte Carlo data for a hard-core square-well fluid and for the restricted primitive model electrolyte yield rho(+/-) to +/-1%-2% of rho(c) down to 1 part in 10(4)-10(3) of T(c) (and confirm well Ising character). Pressure mixing in the scaling fields is unequivocally revealed and indicates Yang-Yang ratios R(mu)=-0.04(4) and 0.2(6) for the two models, respectively.

Journal Article↗

PubMed2003

Asymmetric fluid criticality. I. Scaling with pressure mixing.

The thermodynamic behavior of a fluid near a vapor-liquid and, hence, asymmetric critical point is discussed within a general "complete" scaling theory incorporating pressure mixing in the nonlinear scaling fields as well as corrections to scaling. This theory allows for a Yang-Yang anomaly in which mu(")(sigma)(T), the second temperature derivative of the chemical potential along the phase boundary, diverges like the specific heat when T-->T(c); it also generates a leading singular term, /t/(2beta), in the coexistence curve diameter, where t[triple bond](T-T(c))/T(c). The behavior of various special loci, such as the critical isochore, the critical isotherm, the k-inflection loci, on which chi((k))[triple bond]chi(rho,T)/rho(k) (with chi=rho(2)k(B)TK(T)) and C((k))(V)[triple bond]C(V)(rho,T)/rho(k) are maximal at fixed T, is carefully elucidated. These results are useful for analyzing simulations and experiments, since particular, nonuniversal values of k specify loci that approach the critical density most rapidly and reflect the pressure-mixing coefficient. Concrete illustrations are presented for the hard-core square-well fluid and for the restricted primitive model electrolyte. For comparison, a discussion of the classical (or Landau) theory is presented briefly and various interesting loci are determined explicitly and illustrated quantitatively for a van der Waals fluid.

Journal Article↗