Molecular structure and interfacial behaviour of polymers

The aim of this study was to investigate the influence of the molecular structure on the interfacial behaviour of polymers. Theoretical models were developed for three different systems. All these models are based on the self-consistent field theory of Scheutjens and Fleer for the adsorption of homopolymers.This self-consistent field theory is a lattice model. All possible polymer conformations on the lattice are taken into account. The potential of a conformation is sum of the local potentials of the segments of the molecule. In each layer a mean field approximation is used to calculate the mixing energy. The volume fraction profile is determined by the segmental potentials and vice versa. A numerical method is used to solve the obtained set of equations.In chapter 2 the influence of association of block copolymers on adsorption is considered. In order to model spherical aggregates (micelles), the planar lattice, as used for modelling planar aggregates (membranes) and adsorption on flat surfaces, is replaced by a spherical lattice. The equilibrium solution concentration in a micellar solution is determined by a small system thermodynamics argument. The adsorption of diblock copolymers with long lyophobic and short lyophilic blocks shows strongly cooperative effects. A single molecular layer is present if the lyophobic block adsorbs. The adsorption isotherm shows an S-shape at the onset of adsorption. A strong increase of the adsorbed amount occurs near the cmc and above the cmc the adsorbed amount is almost constant. A bilayer at the surface can be formed if the lyophilic block adsorbs. Adsorption of the lyophilic blocks would expose the insoluble blocks to the solvent. Therefore, a second layer of molecules adsorbs with their lyophobic block towards the molecules attached to the surface. The influence of the interaction energies and the block sizes on these trends is described. The results obtained show good qualitative agreement with experimental results on surfactant adsorption.The adsorption of random copolymers from solution is described in chapter 3. Experimentally, random copolymers are usually very polydisperse, both in chain length and in primary structure. Random copolymers which are only polydisperse in primary structure are considered here. They can be prepared experimentally by random chemical modification of monomer units of monodisperse homopolymers. The sequence distribution of random copolymers is determined by the fractions of the segment types in the polymer and the correlation factors between them. For random copolymers consisting of two different segment types, a blockiness parameter B is defined. The extremes of this parameter are -1 and 1, where the lower limit depends on the fractions of the different segment types. A value of B = -1 represents an alternating copolymer, whereas B = 1 stands for a mixture of two homopolymers. The complete statistical sequence distribution is implemented into the theory. In the results section random copolymers with two different segment types are studied. Chains with a higher than average content of adsorbing segments are preferentially adsorbed from the bulk solution. Only in the first few layers near the surface this preferential effect plays a role. In the remainder of the profile the segment types are more randomly mixed. The adsorption behaviour of these random copolymers is remarkably different from the adsorption of diblock copolymers. In the latter case, the chains have their adsorbing segments mainly in the layers near the surface, whereas further away from the surface long dangling tails of nonadsorbing segments are found. Random copolymers cannot spacially separate their segments so easily. Much higher adsorbed amounts are found for diblock copolymers than for random copolymers with the same fraction of adsorbing segments. The adsorption of random copolymers is less than that of homopolymer of equal length and consisting of the same type of adsorbing segments. Only for very high adsorption energies the adsorbed amounts are essentially the same. An increase in the blockiness parameter of the chains gives an higher adsorbed amount, but it is always below the adsorbed amount of the homopolymer. Analytical expressions have been derived which relate the interaction parameters of purely random copolymer and homopolymer.In chapter 4 the interactions between surfaces coated with grafted polymer (also called hairy plates or soft surfaces) in the presence of nonadsorbing polymer is studied. The interaction free energy between the surfaces is obtained from the partition function. which is rederived for this more general case. For hard plates the interaction is fully determined by the osmotic pressure of the bulk solution and the depletion layer thickness. However. It turns out that In the case of soft surfaces the hairs have an attractive contribution to the free energy of interaction at a plate separation just below twice the hydrodynamic layer thickness of the grafted layer. The hairs mix mutually more easily than with free polymer. At a larger overlap of hairs the interaction becomes repulsive. In contrast with bare planar surfaces, the free energy of interaction between hairy surfaces shows a minimum as a function of the concentration of free polymer in the bulk solution. At a certain (very low) surface coverage the attraction is minimal. For even lower and for larger grafting densities the plates become more attractive. Increasing the repulsion between the hairs and free polymer makes the attraction stronger. The solvencies of grafted and free polymer have a less pronounced effect. Without free polymer, the interaction between the hairy surfaces becomes attractive if the solvency becomes worse than theta conditions.It can be concluded that the self-consistent field theory has been successfully extended to three rather complex but technologically relevant systems. In this way a better understanding of the behaviour of polymers near interfaces has been obtained

Quantum dynamics, dissipation, and asymmetry effects in quantum dot arrays

We study the role of dissipation and structural defects on the time evolution of quantum dot arrays with mobile charges under external driving fields. These structures, proposed as quantum dot cellular automata, exhibit interesting quantum dynamics which we describe in terms of equations of motion for the density matrix. Using an open system approach, we study the role of asymmetries and the microscopic electron-phonon interaction on the general dynamical behavior of the charge distribution (polarization) of such systems. We find that the system response to the driving field is improved at low temperatures (and/or weak phonon coupling), before deteriorating as temperature and asymmetry increase. In addition to the study of the time evolution of polarization, we explore the linear entropy of the system in order to gain further insights into the competition between coherent evolution and dissipative processes.Comment: 11pages,9 figures(eps), submitted to PR

Home ranges, movements and spatial relationships in an expanding population of black rhinoceros

Over 3000 sightings and fixes of individually identified black rhinoceros (Diceros bicornis minor ) over a 14-year period provided information on the spatial organization and movements of these introduced animals and their offspring in the Great Fish River Reserve, South Africa. Core home ranges based on 50% adaptive kernel calculations proved useful for depicting spatial associations among individuals and shifts in areas of occupation. The mean home range size (minimum convex polygon) was 11.7 km 2 and that of core adaptive kernel 6.8 km 2 . Annual and individual variations in home range size were great and social factors clearly affected size. For these and other reasons great caution is recommended in interpretation and inter-population comparisons of home range sizes. Most individuals in this expanding population showed mobility, with home ranges shifting over time. Although clearly exhibiting individual home ranges, most females associated in clusters of three or more individuals. Calves generally moved away from their mothers at the time of her next calving, but some subsequently moved back into their mothers' core home range. In addition to mother-offspring pairs, some females also showed multiple-year associations in these clusters. Male home ranges overlapped, and individuals showed multiple-year associations until they reached approximately nine years of age. Males over age 8 were rarely sighted in the core home range of other similarly aged males

Conductance of tubular nanowires with disorder

We calculate the conductance of tubular-shaped nanowires having many potential scatterers at random positions. Our approach is based on the scattering matrix formalism and our results analyzed within the scaling theory of disordered conductors. When increasing the energy the conductance for a big enough number of impurities in the tube manifests a systematic evolution from the localized to the metallic regimes. Nevertheless, a conspicuous drop in conductance is predicted whenever a new transverse channel is open. Comparison with the semiclassical calculation leading to purely ohmic behavior is made.Comment: 8 pages, 5 figure

Route following without scanning

Desert ants are expert navigators, foraging over large distances using visually guided routes. Recent models of route following can reproduce aspects of route guidance, yet the underlying motor patterns do not reflect those of foraging ants. Specifically, these models select the direction of movement by rotating to find the most familiar view. Yet scanning patterns are only occasionally observed in ants. We propose a novel route following strategy inspired by klinokinesis. By using familiarity of the view to modulate the magnitude of alternating left and right turns, and the size of forward steps, this strategy is able to continually correct the heading of a simulated ant to maintain its course along a route. Route following by klinokinesis and visual compass are evaluated against real ant routes in a simulation study and on a mobile robot in the real ant habitat. We report that in unfamiliar surroundings the proposed method can also generate ant-like scanning behaviours

Flat-band ferromagnetism in quantum dot superlattices

Possibility of flat-band ferromagnetism in quantum dot arrays is theoretically discussed. By using a quantum dot as a building block, quantum dot superlattices are possible. We consider dot arrays on Lieb and kagome lattices known to exhibit flat band ferromagnetism. By performing an exact diagonalization of the Hubbard Hamiltonian, we calculate the energy difference between the ferromagnetic ground state and the paramagnetic excited state, and discuss the stability of the ferromagnetism against the second nearest neighbor transfer. We calculate the dot-size dependence of the energy difference in a dot model and estimate the transition temperature of the ferromagnetic-paramagnetic transition which is found to be accessible within the present fabrication technology. We point out advantages of semiconductor ferromagnets and suggest other interesting possibilities of electronic properties in quantum dot superlattices.Comment: 15 pages, 7 figures (low resolution). High-resolution figures are available at http://www.brl.ntt.co.jp/people/tamura/Research/PublicationPapers.htm

FcgammaR expression on macrophages is related to severity and chronicity of synovial inflammation and cartilage destruction during experimental immune-complex-mediated arthritis (ICA)

INTRODUCTION: Fcγ receptors (FcγRs) present on cells of the haematopoietic lineage communicate with IgG-containing immune complexes that are abundant in the synovial tissue of patients with rheumatoid arthritis (RA). In mice, three classes of FcγR (RI, RII, and RIII) have been described. Binding of these receptors leads to either activation (FcγRI and RIII) or deactivation (FcγRII) of intracellular transduction pathways. Together, the expression of activating and inhibitory receptors is thought to drive immune-complex-mediated diseases. Earlier studies in our laboratory showed that macrophages of the synovial lining are of utmost importance in the onset and propagation of immune-complex-driven arthritic diseases. Selective depletion of macrophages in the joint downregulated both inflammation and cartilage destruction. As all three classes of FcγR are expressed on synovial macrophages, these cells are among the first that come in contact with immune complexes deposited in the joint. Recently, we observed that when immune complexes were injected into the knee joints of mice, strains susceptible to collagen-type-II arthritis (DBA/1, B10.RIII) developed more severe arthritis than nonsusceptible strains did, or even developed chronic arthritis. One reason why these strains are more susceptible might be their higher levels of FcγRs on macrophage membranes. To test this hypothesis, we investigated the role of FcγRs in inflammation and cartilage damage during immune-complex-mediated arthritis (ICA). First, we studied arthritis and subsequent cartilage damage in mice lacking functional FcγRI and RIII (FcR γ-chain(-/-) mice). Next, DBA/1 mice, which are prone to develop collagen-type-II arthritis (`collagen-induced arthritis'; CIA) and are hypersensitive to immune complexes, were compared with control C57BL/6 mice as regards cartilage damage and the expression and function of FcγRs on their macrophages. AIMS: To examine whether FcγR expression on macrophages is related to severity of synovial inflammation and cartilage destruction during immune-complex-mediated joint inflammation. METHODS: ICA was induced in three strains of mice (FcR γ-chain(-/-), C57BL/6, and DBA/1, which have, respectively, no functional FcγRI and RIII, intermediate basal expression of FcγRs, and high basal expression of FcγRs) by passive immunisation using rabbit anti-lysozyme antibodies, followed by poly-L-lysine lysozyme injection into the right knee joint 1 day later. In other experiments, streptococcal-cell-wall (SCW)- or zymosan-induced arthritis was induced by injecting SCW (25 μg) or zymosan (180 μg) directly into the knee joint. At several time points after arthritis induction, knee joints were dissected and studied either histologically (using haematoxylin/eosin or safranin O staining) or immuno-histochemically. The arthritis severity and the cartilage damage were scored separately on an arbitrary scale of 0-3. FcγRs were immunohistochemically detected using the monoclonal antibody 2.4G2, which detects both FcγRII and RIII. Deposition of IgG and C3c in the arthritic joint tissue was also detected immunohistochemically. Expression of FcγRs by murine peritoneal macrophages was measured using a fluorescence-activated cell sorter (FACS). Peritoneal macrophages were stimulated using heat-aggregated gamma globulins (HAGGs), and production of IL-1 was measured using a bioassay. To assess the levels of IL-1 and its receptor antagonist (IL-1Ra) during arthritis, tissue was dissected and washed in RPMI medium. Washouts were tested for levels of IL-1 and IL-1Ra using radioimmunoassay and enzyme-linked immunosorbent assay. mRNA was isolated from the tissue, and levels of macrophage inflammatory protein (MIP)-2, monocyte chemoattractant protein (MCP)-1, IL-1, and IL-1Ra were determined using semiquantitative reverse-transcription polymerase chain reaction (RT-PCR). RESULTS: ICA induced in knee joints of C57BL/6 mice caused a florid inflammation at day 3 after induction. To investigate whether this arthritis was FcγR-mediated, ICA was induced in FcR γ-chain(-/-) mice, which lack functional FcγRI and RIII. At day3, virtually no inflammatory cells were found in their knee joints. Levels of mRNA of IL-1, IL-1Ra, MCP-1, and MIP-2, which are involved in the onset of this arthritis, were significantly lower in FcR γ-chain(-/-) mice than in control C57BL/6 mice. Levels of IL-1 protein were also measured. At 6 h after ICA induction, FcR γ-chain(-/-) mice and control C57BL/6 mice showed similar IL-1 production as measured by protein level. By 24 h after induction, however, IL-1 production in the FcR γ-chain(-/-) mice was below the detection limit, whereas the controls were still producing a significant amount. To investigate whether the difference in reaction to immune complexes between the DBA/1 and C57BL/6 mice might be due to variable expression of FcγRs in the knee joint, expression in situ of FcγRs in naïve knee joints of these mice was determined. The monoclonal antibody 2.4G2, which detects both FcγRII and RIII, stained macrophages from the synovial lining of DBA/1 mice more intensely than those from C57BL/6 mice. This finding suggests a higher constitutive expression of FcγRs by macrophages of the autoimmune-prone DBA/1 mice. To quantify the difference in FcγR expression on macrophages of the two strains, we determined the occurrence of FcγRs on peritoneal macrophages by FACS analysis. The levels of FcγR expressed by macrophages were twice as high in the DBA/1 mice as in the C57BL/6 mice (mean fluorescence, respectively, 440 ± 50 and 240 ± 30 intensity per cell). When peritoneal macrophages of both strains were stimulated with immune complexes (HAGGs), we found that the difference in basal FcγR expression was functional. The stimulated macrophages from DBA/1 mice had significantly higher IL-1α levels (120 and 135 pg/ml at 24 and 48 h, respectively) than cells from C57BL/6 mice (45 and 50 pg/ml, respectively). When arthritis was induced using other arthritogenic triggers than immune complexes (zymosan, SCW), all the mouse strains tested (DBA/1, FcR γ-chain(-/-), and C57BL/6) showed similar inflammation, indicating that the differences described above are found only when immune complexes are used to elicit arthritis. We next compared articular cartilage damage in arthritic joints of the three mouse strains FcR γ-chain(-/-), C57BL/6 (intermediate basal expression of FcγRs), and DBA/1 (high basal expression of FcγRs). Three indicators of cartilage damage were investigated: depletion of PGs, chondrocyte death, and erosion of the cartilage matrix. At day 3 after induction of ICA, there was no PG depletion in FcR γ-chain(-/-) mice, whereas PG depletion in the matrix of the C57BL/6 mice was marked and that in the arthritic DBA/1 mice was even greater. PG depletion was still massive at days 7 and 14 in the DBA/1 mice, whereas by day 14 the PG content was almost completely restored in knee joints of the C57BL/6 mice. Chondrocyte death and erosion of cartilage matrix, two indicators of more severe cartilage destruction, were significantly higher in the DBA/1 than in the C57BL/6 mice, while both indicators were completely absent in the FcR γ-chain(-/-) mice. Again, when arthritis was induced using other triggers (SCW, zymosan), all strains showed similar PG depletion and no chondrocyte death or matrix erosion. These findings underline the important role of immune complexes and FcγRs in irreversible cartilage damage. DISCUSSION: Our findings indicate that inflammation and subsequent cartilage damage caused by immune complexes may be related to the occurrence of FcγRs on macrophages. The absence of functional FcγRI and RIII prevented inflammation and cartilage destruction after induction of ICA, whereas high basal expression of FcγRs on resident joint macrophages of similarly treated mice susceptible to autoimmune arthritis was correlated with markedly more synovial inflammation and cartilage destruction. The difference in joint inflammation between the three strains was not due to different susceptibilities to inflammation per se, since intra-articular injection of zymosan or SCW caused comparable inflammation. Although extensive inflammatory cell mass was found in the synovium of all strains after intra-articular injection of zymosan, no irreversible cartilage damage (chondrocyte death or matrix erosion) was found. ICA induced in C57BL/6 and DBA/1 mice did cause irreversible cartilage damage at later time points, indicating that immune complexes and FcγRs play an important role in inducing irreversible cartilage damage. Macrophages communicate with immune complexes via Fcγ receptors. Absence of functional activating receptors completely abrogates the synovial inflammation, as was shown after ICA induction in FcR γ-chain(-/-) mice. However, the γ-chain is essential not only in FcγRI and RIII but also for FcεRI (found on mast cells) and the T cell receptor (TcR)-CD3 (Tcells) complex of γδT cells. However, T, B, or mast cells do not play a role in this arthritis that is induced by passive immunisation. Furthermore, this effect was not caused by a difference in clearance of IgG or complement deposition in the tissue. In this study, DBA/1 mice, which are susceptible to collagen-induced autoimmune arthritis and in a recent study have been shown to react hypersensitively to immune complexes, are shown to express higher levels of FcγRs on both synovial and peritoneal macrophages. Because antibodies directed against the different subclasses of FcγR are not available, no distinction could be made between FcγRII and RIII. Genetic differences in DBA/1 mice in genes coding for or regulating FcγRs may be responsible for altered FcγR expression. If so, these mouse strains would have a heightened risk for immune-complex-mediated diseases. To provide conclusive evidence for the roles of the various classes of FcγR during ICA, experiments are needed in which FcγRs are blocked with specific antibodies, or in which knockout mice lacking one specific class of FcγR are used. The only available specific antibody to FcγR (2.4G2) has a stimulatory effect on cells once bound to the receptor, and therefore cannot be used in blocking experiments. Experiments using specific knockout mice are now being done in our laboratory. Macrophages are the dominant type of cell present in chronic inflammation during RA and their number has been shown to correlate well with severe cartilage destruction. Apart from that, in humans, these synovial tissue macrophages express activating FcRs, mainly FcγIIIa, which may lead to activation of these macrophages by IgG-containing immune complexes. The expression of FcRs on the surface of these cells may have important implications for joint inflammation and severe cartilage destruction and therefore FCRs may constitute a new target for therapeutic intervention