A new free volume model for dynamic viscosity of dense fluids versus pressure and temperature. Extension to a predictive model for not very associative mixtures

cited By 4International audienceThis article presents the extension of a viscosity model to mixtures. This model, based on the free volume concept, has been previously validated for pure dense components. This model involves three physical constants for each pure compound. If the viscosity is known at a reference pressure and temperature it is sufficient to use two constants per pure compound. The model has been adapted in order to obtain a predictive expression able to represent with accuracy the pressure-temperature variations of the dynamic viscosity of a mixture knowing only the characteristic parameters of each pure compound and the composition. The database used contains 3440 data points relative to 15 binaries, 4 ternaries and I system with more than three constituents. The model's results are also compared with those calculated from the very well-known Grunberg and Nissan's mixing law, and Katti and Chaudhri's mixing law

CCKA, but not CCKB, agonists suppress the hyperlocomotion induced by endogenous enkephalins, protected from enzymatic degradation by systemic RB 101

International audienceInteractions between CCKergic and enkephalinergic systems were studied in mice using behavioral responses measured in Animex. The hyperlocomotion induced by 5 mg/kg of RB 101, a mixed inhibitor of enkephalin-degrading enzymes able to cross the blood-brain barrier, was previously shown to be mediated by delta-opioid receptor stimulation. The IP administration of a CCKA agonist, Boc-Tyr-Lys-(CONH-o-tolyl)-Asp-Phe-NH2 (0.1, 1, 10 micrograms/kg), suppressed the hyperlocomotion produced by IV injection of 5 mg/kg of RB 101. The effect of the CCKA agonist was suppressed by a selective CCKA antagonist, devazepide, injected IP at doses of 20 and 200 micrograms/kg and was potentiated by the selective delta-opioid antagonist naltrindole at the doses of 0.03 mg/kg. IP injection of the selective CCKB agonist BC 264 (0.1-1 mg/kg) did not modify the RB 101-induced hyperlocomotor effect. These results reinforce the observed physiological antagonism between the endogenous CCK and opioid systems but are at variance with the responses measured in stressful conditions. It is concluded that CCKA, but not CCKB, receptor activation counteracts the opioid-related hyperlocomotion

Novel approaches in the development of new analgesics

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The chemokine stromal cell-derived factor-1/CXCL12 activates the nigrostriatal dopamine system.

We recently demonstrated that dopaminergic (DA) neurons of the rat substantia nigra constitutively expressed CXCR4, receptor for the chemokine stromal cell-derived factor-1 (SDF-1)/CXCL12 (SDF-1). To check the physiological relevance of such anatomical observation, in vitro and in vivo approaches were used. Patch clamp recording of DA neurons in rat substantia nigra slices revealed that SDF-1 (10 nmol/L) induced: (i) a depolarization and increased action potential frequency; and (ii) switched the firing pattern of depolarized DA neurons from a tonic to a burst firing mode. This suggests that SDF-1 could increase DA release from neurons. Consistent with this hypothesis, unilateral intranigral injection of SDF-1 (50 ng) in freely moving rat decreased DA content and increased extracellular concentrations of DA and metabolites in the ipsilateral dorsal striatum, as shown using microdialysis. Furthermore, intranigral SDF-1 injection induced a contralateral circling behavior. These effects of SDF-1 were mediated via CXCR4 as they were abrogated by administration of a selective CXCR4 antagonist. Altogether, these data demonstrate that SDF-1, via CXCR4, activates nigrostriatal DA transmission. They show that the central functions of chemokines are not restricted, as originally thought, to neuroinflammation, but extend to neuromodulatory actions on well-defined neuronal circuits in non-pathological conditions

Enhancement of the effects of a complete inhibitor of enkephalin-catabolizing enzymes, RB 101, by a cholecystokinin-B receptor antagonist in diabetic rats

1. RB 101, a complete inhibitor of enkephalin-catabolizing enzymes, has been previously shown to produce antinociception in normal rats after systemic administration. Moreover, its coadministration with a cholecystokinin-B (CCK-B) receptor antagonist has been shown to strongly enhance its antinociceptive effect in normal rats. In this work, we determined whether RB 101 was able to reduce hyperalgesia and allodynia in diabetic rats, a model of neuropathic pain. The type of opioid receptors (μ or δ) involved was determined using naloxone and naltrindole, respectively, and the interactions between endogenous enkephalins and CCK on nociception control was investigated using coadministration of RB 101 and the CCK-B receptor antagonist CI-988. 2. RB 101 suppressed mechanical hyperalgesia (paw pressure-induced vocalization test), partially alleviated mechanical allodynia (von Frey hair test), and was ineffective in thermal allodynia (tail immersion test). The analgesic effect was completely cancelled by naloxone or naltrindole, suggesting that is requires the availability of μ- and/or δ-opioid receptors. 3. The combination of an inactive dose of CI-988 with the lowest effective dose of RB 101 resulted in a stronger increase in the vocalization threshold comparatively to RB 101 alone. 4. The present study demonstrates that the antinociception generated by RB 101 induced by elevation of extracellular levels of endogenous enkephalins, can be extended to neuropathic pain in diabetic rats and that blockade of CCK-B receptors potentiated antinociceptive effects elicited by RB 101

Viscosity measurements and correlations of binary mixtures: 1,1,1,2-tetrafluoroethane (HFC-134a)+tetraethylene glycol dimethylether (TEGDME)

International audienceThis paper reports viscosity data for the binary system1,1,1,2- tetrafluoroethane (HFC-134a), x1, +tetraethylene glycol dimethylether (TEGDME), 1 - x1. The measurements (200 data points) were obtained at various pressures (between 10 and 100 MPa) in the homogeneous liquid state from T = 293.15-373.15 K. The measurements have been carried out with a falling body viscometer for four molar fractions x1 = (0.28, 0.44, 0.63 and 0.88). The density values of this system were interpolated from previous results obtained at the laboratory. All of the available viscosity data, including pure HFC-134a and pure TEGDME (both previously studied at the laboratory), have been correlated using several viscosity models (mixing rules, self-refrencing model, hard-sphere theory, friction theory and free volume model). The resulting models are presented and discussed in this work