The primary objective of the present study is to clarify the droplet disintegration mechanism and the film properties of liquid oil films driven by shear stress, which is induced by a co-current gas flow. This work focuses on the flow behavior within the starting length of the complex two-phase flow and the effect of inclination on the entrainment rate. Many investigations have been performed in the past to determine the droplet entrainment in the gas core for fully developed flow conditions with respect to their relevance in pipes of power plants and various chemical engineering systems. In more recent work the effect of inclination has been studied in detail. Nevertheless, a lack of knowledge can be realized for droplet entrainment within the starting length of this complex flow type. Thus, fundamental experiments have been carried out to provide a data base for droplet entrainment of liquid disintegrated from an oil film within its starting length at several inclination angles of the flow. The experimental results have been compared with correlations from literature. Additionally, the wall film thickness has been measured to allow a fully coupled modeling of entrainment and liquid film properties depending on global flow parameters. Based on film Reynolds number Weber number a dimensionless film flow length, and a modified Froude number, taking into account the angle of inclination, correlations have been developed, where those from literature are not applicable.

Glutamine is one major precursor of gamma-aminobutyric acid (GABA) and glutamate, the most important inhibitory and excitatory neurotransmitters in the mammalian brain, respectively. Changes in cerebral glutamine concentrations occur in various metabolic encephalopathies including hyperammonemia and liver failure. As glutamine inhibits the specific binding of GABA to its postsynaptic receptor at physiologic concentrations, in this study the effects of glutamine on various components of the GABAA-benzodiazepine receptor complex were studied. Glutamine dose dependently inhibited the stimulation of flunitrazepam binding by GABA. This inhibition occurred already at concentrations of 10 mumol/L glutamine. Glutamine had no effects on basal or GABA-stimulated synaptoneurosomal chloride uptake. It is concluded that glutamine is not a modulator of the GABAA-benzodiazepine neurotransmitter system. Thus, changes of cerebral glutamine concentrations are unlikely to contribute to the activation of GABA-ergic neurotransmission in liver failure.

An imbalance of excitatory and inhibitory amino acid-ergic neurotransmission has been suggested to play a role in the pathogenesis of hepatic encephalopathy. For further evaluation of this hypothesis, several parameters of amino acid-ergic neurotransmission were studied in rats with acute liver failure induced by the administration of 300 mg per kg thioacetamide by gavage on two consecutive days. By appropriate supportive care, hypoglycemia, renal failure and hypothermia were avoided. Rats were monitored clinically and neurologically. Hepatic encephalopathy evolved in four distinct, easily recognizable stages. Light and electron microscopic examination of brains of rats with hepatic encephalopathy revealed only a slight swelling of nuclei of neurons and astrocytes without signs of neuronal degeneration or brain edema. In rats with hepatic encephalopathy, the concentrations of GABA, glutamate and taurine were decreased in the cerebral cortex, the hippocampus and the striatum, whereas those of aspartate and glycine were unchanged or increased. GABAA and benzodiazepine receptors were studied as parameters for the postsynaptic GABAA-benzodiazepine receptor complex, glutamic acid decarboxylase as parameter for presynaptic GABA-ergic neurons and stimulation of benzodiazepine binding by GABA as a parameter for a GABA-mediated postsynaptic event. None of these parameters was different in hepatic encephalopathy as compared to controls. Similarly, Ca++/Cl(-)-dependent and -independent glutamate receptors as parameters for glutamatergic neurons were unchanged in rats with hepatic encephalopathy. Thus, in rats with thioacetamide-induced liver failure and hepatic encephalopathy, changes of the concentrations of neurotransmitter amino acids occur in the brain. Other neurochemical parameters, however, failed to identify alterations of GABA-ergic or glutamatergic neurotransmission in hepatic encephalopathy.

Serum concentrations of gamma-aminobutyric acid (GABA) are increased in liver failure, possibly because of decreased hepatic GABA catabolism. To study in detail the role of the liver in GABA metabolism, uptake and catabolism of GABA by isolated perfused liver from normal rats and rats with galactosamine- or carbon tetrachloride-induced liver failure were measured. Hepatic GABA uptake was almost complete at GABA concentrations of up to 10 microM and approached saturation at a concentration of 50 microM. The apparent affinity of hepatic GABA uptake was 38 microM and the apparent maximal velocity was 158 nmol/g.min. Hepatic GABA uptake was sodium-dependent. gamma-Aminobutyric acid taken up by the liver was rapidly catabolized as measured by 14CO2 formation from [U-14C]GABA. Aminooxyacetic acid, a GABA transaminase inhibitor, completely and irreversibly inhibited hepatic GABA catabolism and thereby also inhibited hepatic GABA uptake. Although uptake of GABA by livers of carbon tetrachloride- or galactosamine-treated rats was decreased (apparent maximal velocity, 103 and 98 nmol/g.min, respectively), at physiologic GABA concentrations in the perfusate GABA uptake and catabolism was not different from that of untreated controls. The observed impairment of hepatic GABA uptake or catabolism by the diseased liver would be expected to contribute to increased GABA levels in peripheral blood plasma in liver failure. However, the magnitude of the observed impairment would be insufficient to account for a 10-fold increase in such levels.

Optical-absorption coefficient data are presented over the 0.7--1.5-eV spectral range (825--1750 nm) for ${\mathrm{In}}_{1\mathrm{\ensuremath{-}}\mathrm{x}}$${\mathrm{Ga}}_{\mathrm{x}}$As/InP; both at the lattice-matched condition x=0.47 and for the 0.45<x<0.51 composition range. Absorption data for such epilayers are compared at 10, 77, and 300 K. This comparison involves numerous epilayers grown by organometallic vapor-phase epitaxy, a lattice-matched layer grown by molecular-beam epitaxy, and published data for ${\mathrm{In}}_{1\mathrm{\ensuremath{-}}\mathrm{x}}$${\mathrm{Ga}}_{\mathrm{x}}$As grown by liquid-phase epitaxy. It is demonstrated that these growth techniques yield material with equivalent absorption characteristics. For all compositions, the absorption coefficient \ensuremath{\alpha}(h\ensuremath{\nu}) rises abruptly to near 6000 ${\mathrm{cm}}^{\mathrm{\ensuremath{-}}1}$ at the band gap, and increases more gradually to 30 000 ${\mathrm{cm}}^{\mathrm{\ensuremath{-}}1}$ at 1.5 eV. For energies above 1.3 eV, all the ${\mathrm{In}}_{1\mathrm{\ensuremath{-}}\mathrm{x}}$${\mathrm{Ga}}_{\mathrm{x}}$As epilayers studied here show essentially the same absorption characteristics, regardless of composition or temperature.

The specific binding of γ-aminobutyric acid (GABA) to synaptic membranes prepared from the brains of rats with acute liver failure due to portacaval shunt and hepatic artery ligation was measured. No changes in the affinity or the density of the low- and high-affinity binding sites of the GABA receptor were observed, indicating that this model of acute hepatic encephalopathy is apparently not associated with altered GABAergic neurotransmission.

The progressive course of hepatic encephalopathy developing in rats after massive hepatic ischemia due to hepatic artery ligation within 48 hr of a portacaval shunt was not altered by the injection of a benzodiazepine antagonist, CGS 8216, in a dose that was sufficient to reverse diazepam-induced coma quickly. The onset of hepatic coma was shortened 20 to 25% by the antagonist, rather than being delayed, as would be expected if hepatic coma were due to a γ-aminobutyric acid (GABA)-ergic effect. The neural binding of GABA by brains from rats in deep hepatic coma was unaffected by the injection of the benzodiazepine antagonist.