Vapour–Liquid Equilibria in the Polystyrene + Toluene System at Higher Concentrations of Solvent

Vapour–liquid equilibria (VLE) were determined in the polystyrene + toluene system under isothermal conditions at 363.15, 373.15, and 383.15 K using an improved all-glass microebulliometer with circulation of the liquid phase for the dynamic measurement of total pressure over liquid mixtures. The experimental data were correlated using the UNIQUAC-free volume model and the applicability of three known predictive models was tested. It was found that prediction of VLE using the GC-Flory equation of state, the UNIFAC-vdw-FV and the Entropic-FV model are of the same quality

Vapour–Liquid Equilibria in the Poly(methyl methacrylate) + 2-Butanone System Containing Lower Concentrations of Solute at Normal or Reduced Pressures

Vapour–liquid equilibria (VLE) were determined in the poly(methyl methacrylate) + 2-butanone system under isothermal conditions at 333.15, 343.15, and 353.15 K using an improved all-glass micro-ebulliometer with circulation of the liquid phase for the dynamic measurement of total pressure over liquid mixtures. The experimental data were correlated using the UNIQUAC-FV model and the applicability of three known predictive models was tested. It was found that only the UNIFAC-vdw-FV model gives excellent prediction of VLE for the studied system

Azeotropic Behavior of the 2-Methylpropan-2-ol + water + 1-ethyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide System

Vapor-liquid equilibrium data were measured isothermally in the near-azeotropic region of the 2-methylpropan-2-ol + water + 1-ethyl-3-methylimidazolium bis(trifluoromethylsulfonyl) imide system at 333.15, 343.15, and 353.15 K. The data were processed using a recently developed method based on a small number of experiments that provides a complete thermodynamic description of the azeotropic behavior. The parameters of the third-order Redlich-Kister equation were correlated with the ionic liquid concentration to determine an analytical dependence of both the azeotropic composition and the pressure

Saltatory remodeling of Hox chromatin in response to rostrocaudal patterning signals

Hox genes controlling motor neuron subtype identity are expressed in rostrocaudal patterns that are spatially and temporally collinear with their chromosomal organization. Here we demonstrate that Hox chromatin is subdivided into discrete domains that are controlled by rostrocaudal patterning signals that trigger rapid, domain-wide clearance of repressive histone H3 Lys27 trimethylation (H3K27me3) polycomb modifications. Treatment of differentiating mouse neural progenitors with retinoic acid leads to activation and binding of retinoic acid receptors (RARs) to the Hox1–Hox5 chromatin domains, which is followed by a rapid domain-wide removal of H3K27me3 and acquisition of cervical spinal identity. Wnt and fibroblast growth factor (FGF) signals induce expression of the Cdx2 transcription factor that binds and clears H3K27me3 from the Hox1–Hox9 chromatin domains, leading to specification of brachial or thoracic spinal identity. We propose that rapid clearance of repressive modifications in response to transient patterning signals encodes global rostrocaudal neural identity and that maintenance of these chromatin domains ensures the transmission of positional identity to postmitotic motor neurons later in development.Leona M. and Harry B. Helmsley Charitable TrustNational Institutes of Health (U.S.) (Grant P01 NS055923)Smith Family Foundatio

Neuromuscular Junction Defects in Mice with Mutation of dynein heavy chain 1

Disruptions in axonal transport have been implicated in a wide range of neurodegenerative diseases. Cramping 1 (Cra1/+) and Legs at odd angles (Loa/+) mice, with hypomorphic mutations in the dynein heavy chain 1 gene, which encodes the ATPase of the retrograde motor protein dynein, were originally reported to exhibit late onset motor neuron disease. Subsequent, conflicting reports suggested that sensory neuron disease without motor neuron loss underlies the phenotypes of Cra1/+ and Loa/+ mice. Here, we present behavioral and anatomical analyses of Cra1/+ mice. We demonstrate that Cra1/+ mice exhibit early onset, stable behavioral deficits, including abnormal hindlimb posturing and decreased grip strength. These deficits do not progress through 24 months of age. No significant loss of primary motor neurons or dorsal root ganglia sensory neurons was observed at ages where the mice exhibited clear symptomatology. Instead, there is a decrease in complexity of neuromuscular junctions. These results indicate that disruption of dynein function in Cra1/+ mice results in abnormal morphology of neuromuscular junctions. The time course of behavioral deficits, as well as the nature of the morphological defects in neuromuscular junctions, suggests that disruption of dynein function in Cra1/+ mice causes a developmental defect in synapse assembly or stabilization