Orthoscopic real-image display of digital holograms.

We present a practical solution for the long-standing problem of depth inversion in real-image holographic display of digital holograms. It relies on a field lens inserted in front of the spatial light modulator device addressed by a properly processed hologram. The processing algorithm accounts for pixel size and wavelength mismatch between capture and display devices in a way that prevents image deformation. Complete images of large dimensions are observable from one position with a naked eye. We demonstrate the method experimentally on a 10-cm-long 3D object using a single full-HD spatial light modulator, but it can supplement most holographic displays designed to form a real image, including circular wide angle configurations.

Extended Mueller-Stokes description of polarization-mode transformation in linearly birefringent single-mode optical fibers.

We derive a more general version of the commonly known quasi-monochromatic Mueller matrix of a linearly birefringent single-mode optical fiber. In the matrix, the complex degree of self-coherence of the illuminating field is replaced by the normalized cross-correlation of a pair of any jointly stationary light disturbances associated with the eigenpolarization modes, where both modulus and phase of the cross correlation are included. This allows one to write polychromatic Mueller-Stokes equations of multisection systems transmitting any uniformly polarized stationary field. A way for handling arbitrary phase birefringence dispersion is also suggested.

A new virtual reality approach for planning of cardiac interventions.

A novel approach to three-dimensional (3D) visualization of high quality, respiratory compensated cardiac magnetic resonance (MR) data is presented with the purpose of assisting the cardiovascular surgeon and the invasive cardiologist in the pre-operative planning. Developments included: (1) optimization of 3D, MR scan protocols; (2) dedicated segmentation software; (3) optimization of model generation algorithms; (4) interactive, virtual reality visualization. The approach is based on a tool for interactive, real-time visualization of 3D cardiac MR datasets in the form of 3D heart models displayed on virtual reality equipment. This allows the cardiac surgeon and the cardiologist to examine the model as if they were actually holding it in their hands. To secure relevant examination of all details related to cardiac morphology, the model can be re-scaled and the viewpoint can be set to any point inside the heart. Finally, the original, raw MR images can be examined on line as textures in cut-planes through the heart models.

Is the glutathione conjugate of trans-4-hydroxy-2-nonenal transported by the multispecific organic anion transporting-ATPase of human erythrocytes?

Trans-4-hydroxy-2-nonenal (4-HNE), a cytotoxic end product of lipid peroxidation, is present in normal human blood plasma at concentrations of 0.1-1.0 microM. It can be, however, further metabolized within a cell, and one of the main products is 4-HNE glutathione conjugate (HNE-SG). In human erythrocyte membrane the system for active extrusion of glutathione (GSH) conjugates of various endo- and xenobiotics has been described; it exhibits either a low (Km at submillimolar concentration range) or a high (Km at low micromolar range) affinity for the transported substrates, such as for example S-(2,4-dinitrophenyl)glutathione (Dnp-SG). In the present study it has been shown that the high affinity transport system for Dnp-SG is competitively inhibited by HNE-SG with Ki of 0.2 microM, while 4-HNE inhibits non-competitively the activity of the transport system for Dnp-SG with Ki of 220microM. These observations point to the possibility that HNE-SG shares the same transport system with GSH conjugates of other endo- and xenobiotics in erythrocytes. This may be of importance for overall detoxification of the organism under oxidative stress.

An antagonist of ATP-regulated potassium channels, the guanidine derivative U-37883A, stimulates the synthesis of phosphatidylserine in rat liver endoplasmic reticulum membranes.

The guanidine derivative U-37883A has been found to stimulate in vitro synthesis of phosphatidylserine in endoplasmic reticulum membranes, catalyzed exclusively by a serine-specific base exchange enzyme. The stimulation of the enzyme activity by the drug was concentration-dependent, with EC50 of 54 microM, while the biologically inactive analog of U-37883A, U-42069, was without effect. The stimulation caused by U-37883A was enhanced under the conditions when active transport of Ca2+ into the lumen of microsomal vesicles was induced, whereas it was inhibited by a calcium ionophore, A23187, and by a specific inhibitor of Ca2+-ATPase, thapsigargin. On the other hand, a potassium ionophore, valinomycin, had no effect on phosphatidylserine synthesis. U-37883A did not affect the Km of the base exchange enzyme for serine, but greatly reduced the EC50 value of the enzyme for calcium. Furthermore, Ca2+ uptake by endoplasmic reticulum vesicles has been found to increase in the presence of U-37883A. These observations suggest that U-37883A enhances phosphatidylserine synthesis indirectly by acting on calcium transport, thus affecting calcium concentration within the lumen of endoplasmic reticulum membranes. Alternatively, the effect of the drug could be propagated via the mechanism by which phospholipid flip-flop movement, known to regulate the serine-specific base exchange reaction, is modulated.

Membrane integrity and phospholipid movement influence the base exchange reaction in rat liver microsomes.

Properties of Ca(2+)-stimulated incorporation of amincalcohols, serine and ethanolamine, into phospholipids, and factors regulating the reaction were studied in endoplasmic reticulum membranes isolated from rat liver. In contrast to apparent K(m) values for either aminoalcohol, maximal velocities of the reaction were significantly affected by Ca2+ concentration. No competition between these two soluble substrates used at equimolar concentrations close to their K(m) values was observed, suggesting the existence of two distinct phospholipid base exchange activities. The enzyme utilizing the electrically neutral serine was not sensitive to changes of membrane potential evoked by valinomycin in the presence of KCl. On the other hand, when positively charged ethanolamine served as a substrate, the enzyme activity was inhibited by 140 mM KCl and this effect was reversed by valinomycin. The rates of inhibition of phospholipid base exchange reactions by various thiol group modifying reagents were also found to differ. Cd2+ and lipophylic p-chloromercuribenzoic acid at micromolar concentrations were most effective. It can be suggested that -SH groups located within the hydrophobic core of the enzymes molecules are essential for the recognition of membrane substrates. However, the influence of the -SH group modifying reagents on the protein-facilitated phospholipid motion across endoplasmic reticulum membranes can not be excluded, since an integral protein-mediated transverse movement of phospholipids within the membrane bilayer and Ca(2+)-mediated changes in configuration of the phospholipid polar head groups seem to be a regulatory step of the reaction. Indeed, when the membrane integrity was disordered by detergents or an organic solvent, the reaction was inhibited, although not due to the transport of its water-soluble substrates is affected, but due to modulation of physical state of the membrane bilayer and, in consequence, the accessibility of phospholipid molecules.

Interaction of caldesmon with endoplasmic reticulum membrane: effects on the mobility of phospholipids in the membrane and on the phosphatidylserine base-exchange reaction.

We have previously demonstrated by tryptophan fluorescence the interaction of caldesmon with anionic phospholipid vesicles [Czurylo, Zborowski and Dabrowska (1993) Biochem. J. 291, 403-408]. In the present work we investigated the interaction of caldesmon with natural-membrane (rat liver endoplasmic reticulum) phospholipids by co-sedimentation assay. The results indicate that 1 mol of caldesmon binds approx. 170 mol of membrane phospholipids with a binding affinity constant of 7.3 x 10(6) M-1. The caldesmon-membrane phospholipid complex dissociates with increasing salt concentration and in the presence of Ca2+/calmodulin. As indicated by EPR measurements of membrane lipids labelled with 5-doxyl stearate and TEMPO-phosphatidylethanolamine, binding of caldesmon results in an increase in mobility of the acyl chains (in the region of carbon 5) and a decrease in polar headgroup mobility of phospholipids. Interaction of caldesmon with phospholipids is accompanied by inhibition of phosphatidylethanolamine synthesis via a phospholipid base-exchange reaction, with phosphatidylserine as substrate. This shows that, of the endoplasmic reticulum membrane phospholipids, the main target of caldesmon is phosphatidylserine.

The relationship between the binding of ATP and calcium to annexin IV. Effect of nucleotide on the calcium-dependent interaction of annexin with phosphatidylserine.

With the use of ATP analogues, we have found that porcine liver annexin (Anx) IV can be covalently labelled with 8-azido[gamma-32P]-ATP in the presence of Ca2+ (Kd 4.2 microM) and that the labelling is prevented by asolectin/cholesterol liposomes or chelation of calcium ions. On the other hand, non-covalent binding of 2'-(or 3')-O-(2,4,6-trinitrophenyl)adenosine 5'-triphosphate (TNP-ATP) to AnxIV occurs optimally in the presence of liposomes and Ca2+ (Kd 7 microM). These observations were further confirmed by the results of intrinsic fluorescence quenching of AnxIV with various nucleotides, suggesting the existence of a relationship between Ca(2+)-, phospholipid- and ATP-binding sites within the annexin molecule. The interaction of AnxIV with nucleotides does not significantly affect its in vitro properties concerning the binding to phosphatidylserine (PS) monolayers.

Participation of the multispecific organic anion transporter in hepatobiliary excretion of glutathione S-conjugates, drugs and other xenobiotics.

Polarized liver cells, hepatocytes, are involved in carbohydrate, protein and fat metabolism, breakdown of hemoglobin and production of bile. They are also involved in overall detoxification processes in an organism associated with the transport of bile salts, cholesterol, phospholipids, endo- and xenobiotics, end-products of cellular metabolism and ions through the canalicular region of the hepatocyte plasma membrane. Uptake of the above-mentioned compounds into hepatocytes through the basolateral region of plasma membrane is followed by their chemical modification by enzymes of detoxification phase I (e.g. cytochromes P-450) and phase II (e.g. glutathione S-transferases). Canalicular transport participates in phase III of detoxification, and the molecular machinery involved in this process is localized in the canalicular region of the plasma membrane. Canalicular transport includes the following transport systems: a specific canalicular transporter for bile salts, a multidrug resistance 2 P-glycoprotein (MDR2) participating in the transport of lipids, a multidrug resistance 3 P-glycoprotein (MDR3) responsible for the transport of organic cations and the multispecific organic anion transporter (cMOAT) involved in the transport of non-bile acid organic anions. The cMOAT transport system is discussed in this detailed review.

The effect of methadone on fetal brain function.

The effect of methadone on fetal brain function in terms of the electroencephalogram (EEG) was studied in eight short-term fetal sheep experiments by single injections of 5 to 20 mg. of methadone into the fetal circulation. Plasma methadeone concentrations (determined by radioimmunoassay) greater than 0.065 mg. per cent were associated with an immediate brief decrease in carotid blood flow, a rapid decrease in frequency and amplitude in the EEG that occasionally became isoelectric but recovered, and immediate and relatively prolonged bradycardia. Similar cardiovascular observations were obtained with plasma methadone concentrations less than 0.065 mg. per cent, but the EEG changes were either minimal or not observed. These results indicate that uptake of methadone by the fetal brain is rapid and that electrical activity and heart rate are affected.

Effect of alcohol on fetal cerebral function and metabolism.

The effect of maternal alcohol infusions on fetal cerebral function in terms of the electroencephalogram (EEG) and fetal brain metabolism was studied in 10 fetal sheep experiments. A 9.75 per cent alcohol-dextrose solution was infused at the rate of 15 c.c. per kilogram of maternal weight for 1 or 2 hours. Fetal cerebral uptake of oxygen was unaffected. Blood flow was significantly increased as a result of a greater decrease in resistance than decrease in blood pressure. The cerebral uptake of glucose and the glucose-oxygen utilization ratio were significantly increased. The EEG showed a decrease in amplitude and slowing of the dominant rhythm as the blood alcohol concentration increased and became isoelectric on occasion during the postinfusion period associated with a severe fetal acidosis.

Placental transport of alcohol and its effect on maternal and fetal acid-base balance.

The placental transport of alcohol and its effect on maternal and fetal acid-base balance studied in 10 sheep experiments by the maternal infusion of a 9.75 per cent solution of alcohol-dextrose at a rate of 15 c.c. per kilogram for 1 or 2 hours. Serial maternal and fetal blood sampling during and following the alcohol infusion revealed rapid placental diffusion of alcohol, a highly significant correlation between maternal and fetal blood alcohol concentrations, and a similar peak concentration of approximately 0.230 Gm. per 100 ml. in maternal and fetal blood that differed only in time of onset during the 1 and 2 hour infusion periods. Blood alcohol concentrations remained high for several hours during the postinfusion period. A significant maternal hyperlactacidemia and hyperglycemia were noted but did not result in significant alterations in maternal acid-base balance. An initial fetal metabolic acidosis and later mixed acidosis were observed during the alcohol infusion and worsened during the postinfusion period.