New model for the correlation of the surface tension based on friction theory.

A new correlation method for the surface tension of fluids is proposed, which is based on friction theory applied to the interface of a two-phase system. The substance properties enter the model by a regular equation of state. Here we derive the method and test it with the Lennard-Jones 12-6 fluid as the reference system using molecular dynamics simulations of the vapor-liquid interface in combination with a new Lennard-Jones 12-6 equation of state. Further correlations of experimental surface tension data based on the Peng-Robinson and the PC-SAFT equations of state are presented. As a result, we find that the method allows an accurate correlation of the surface tension of pure fluids.

The macrophage-activating lipopeptide-2 accelerates wound healing in diabetic mice.

Wound healing in healthy individuals proceeds at an optimal rate. However, in patients, with -- e.g.-- locally impaired blood flow or diabetes, chronic wounds develop and often become infected. Chronic wounds mean a low quality of life for the afflicted patients, not to mention enormous costs. Rather than using recombinant growth factors to accelerate wound healing, we employed the toll-like receptor agonist macrophage-activating lipopeptide-2 (MALP-2) to improve the healing of full-thickness excision skin wounds in an animal model with obese, diabetic mice. A gene array experiment suggested that MALP-2 stimulates the release of various mediators involved in wound healing. Further data to be presented in this study will show (i) that MALP-2 is capable of stimulating the appearance of the monocyte chemoattractant protein-1 at the wound site, (ii) that this leads to increased leucocyte and, in particular, macrophage infiltration and (iii) that MALP-2-treated wounds closed 2 weeks earlier than vehicle-treated controls. MALP-2, thus, appears to stimulate the early inflammatory process needed to set in motion the ensuing consecutive natural steps of wound healing resulting in wound closure.

Prediction of the thermophysical properties of pure neon, pure argon, and the binary mixtures neon-argon and argon-krypton by Monte Carlo simulation using ab initio potentials.

Gibbs ensemble Monte Carlo simulations were used to test the ability of intermolecular pair potentials derived ab initio from quantum mechanical principles, enhanced by Axilrod-Teller triple-dipole interactions, to predict the vapor-liquid phase equilibria of pure neon, pure argon, and the binary mixtures neon-argon and argon-krypton. The interaction potentials for Ne-Ne, Ar-Ar, Kr-Kr, and Ne-Ar were taken from literature; for Ar-Kr a different potential has been developed. In all cases the quantum mechanical calculations had been carried out with the coupled-cluster approach [CCSD(T) level of theory] and with correlation consistent basis sets; furthermore an extrapolation scheme had been applied to obtain the basis set limit of the interaction energies. The ab initio pair potentials as well as the thermodynamic data based on them are found to be in excellent agreement with experimental data; the only exception is neon. It is shown, however, that in this case the deviations can be quantitatively explained by quantum effects. The interaction potentials that have been developed permit quantitative predictions of high-pressure phase equilibria of noble-gas mixtures.

Mycoplasmal lipopeptide MALP-2 induces the chemoattractant proteins macrophage inflammatory protein 1alpha (MIP-1alpha), monocyte chemoattractant protein 1, and MIP-2 and promotes leukocyte infiltration in mice.

Natural as well as experimental infections with pathogenic mycoplasmas lead to cellular responses characterized by early polymorphonuclear leukocyte influx, which in turn is followed by infiltration of macrophages. Since some of the most potent leukocyte chemoattractants are macrophage products, we investigated whether the 2-kDa macrophage-activating lipopeptide (MALP-2) from Mycoplasma fermentans was capable of inducing chemoattractant chemokines and initiating an in vivo inflammatory effect. MALP-2 was a potent in vitro inducer of the chemokines macrophage inflammatory protein 1alpha (MIP-1alpha), monocyte chemoattractant protein 1 (MCP-1), and MIP-2, yielding a maximal response at 0.1 ng/ml (5 x 10(-11) M). Leukocyte infiltration was determined after intraperitoneal injection of MALP-2, liposome-encapsulated MALP-2, and heat-killed mycoplasmas. There was a steady increase in the number of peritoneal cells over 72 h in response to these agents. Polymorph counts were maximal by 24 to 48 h, decreasing thereafter. Monocytes/macrophages had significantly increased after 3 days. MIP-1alpha, MCP-1, and MIP-2 levels in serum or peritoneal lavage fluid were determined. MIP-1alpha and MCP-1 levels were elevated by 2 to 6 h after injection and were still above control values after 24 h. In contrast, MIP-2 levels reached their maximum at 2 h, dropping to control values after 24 h. We conclude that macrophage-stimulating mycoplasmal lipoproteins, exemplified by MALP-2, play an important role in the late phase of phagocyte recruitment at sites of infection and that this is affected by leukoattractive chemokines.

Activation of nuclear factor-kappaB in macrophages by mycoplasmal lipopeptides.

Mycoplasmas are potent macrophage stimulators. The active principle are lipopeptides or lipoproteins with a characteristic N-terminal S-[dihydroxypropyl]-cysteinyl group bearing two ester-bound fatty acids and lacking the amide-bound one common to other bacterial lipoproteins. Using synthetic analogues of mycoplasmal lipopeptides, we investigated activation of the transcription factor NF-kappaB in the C3H/HeJ mouse-derived DMBM-3 cell line. The lipopeptides activated NF-kappaB at below nanomolar concentrations. Activation in the murine system occurred distinctly earlier than TNF-alpha liberation, excluding autocrine stimulation by TNF-alpha. As determined from a supershift experiment, the active NF-kappaB complex consisted of the heterodimer p50/p65(RelA). The relevance of these findings for the inflammatory response to mycoplasmas and for mycoplasma-mediated effects on HIV-infected macrophages is discussed.