Formation of ordered structures of NO on Rh(111)

In this work, several (unreported) structures of NO on Rh(111) are presented for coverages ranging from 0-0.78 ML. The formation of these structures as evidenced experimentally by scanning tunneling microscopy (STM) images is explained using density-functional theory derived values for the lateral interactions and adsorption energies of NO on Rh(111). Kinetic Monte Carlo simulations using the derived lateral interactions are performed to determine structures at finite temperatures. The resulting structures can be directly compared to the molecular arrangements observed in the STM experiment. The configuration of the first three structures that form for increasing coverage is the same both experimentally and theoretically. In all three structures, the molecules only occupy the fcc and hcp adsorption sites. Yet, at high coverage, at which the top adsorption sites become occupied, a discrepancy arises

NO structures adsorbed on Rh(111) : theoretical approach to high-coverage STM images

Theoretical modeling of scanning tunneling microscopy (STM) measurements is used for the interpretation of images of nitrogen monoxide on Rh(111) surfaces in order to gain insight into the factors which control the contrast of an STM image, especially in the case of high coverage overlayers. Topographic images of NO/Rh(111) for different coverages and adsorption positions were calculated. These results were used to analyze the experimental images obtained for the p(2×2)-3NO and p(3×3)-7NO high coverage structures. The theoretical calculations confirm that not all NO molecules present on the surface can be observed experimentally, the image being dominated by the contribution of top NO molecules in the adlayer. In addition, the calculations reveal that destructive interference effects between molecular contributions in the tunnel current play a decisive role for the different contrast of the two high coverage structures. A general discussion of why and how the differences in the adsorbate surface configuration reflect the experimental STM images is given

Determination of lateral interactions between NO molecules on Rh(111)

. In this study, the STM was used to locally study the adsorption of NO on a Rh(111) single crystal. Three new structures were identified. At 200 K, patches of the (4 × 2)-2NO and an unreported (2 × 2)-2NO structure were found at about 0.50ML coverage. Higher exposure gave rise to a (2 × 2)-3NO structure with all molecules adsorbed in the hcp sites. At 5K, a (4 × 4)-1NO structure was observed. The large separation between the molecules can only arise from repulsive interactions over a distance of at least four times the lattice constant (11 Å). Here the interaction is estimated to be of the order of ~10K or ~0.1 kJ/mol. Dynamic Monte Carlo simulations taking into account adsorption, diffusion and pairwise interactions between adsorbates were used to fit the lateral interaction for the next-next nearest neighbor to the patched STM topograph at 200K for 0.50ML coverage. The value was determined to be 2 kJ/mol. Using pairwise interactions only, the (2 × 2)-3NO structure could not be explained. It might therefore be necessary to include three-particle interactions. Recent DFT calculations support this idea by showing attractive three-particle interactions

Formation of ordered structures of NO on Rh(111)

In this work, several (unreported) structures of NO on Rh(111) are presented for coverages ranging from 0-0.78 ML. The formation of these structures as evidenced experimentally by scanning tunneling microscopy (STM) images is explained using density-functional theory derived values for the lateral interactions and adsorption energies of NO on Rh(111). Kinetic Monte Carlo simulations using the derived lateral interactions are performed to determine structures at finite temperatures. The resulting structures can be directly compared to the molecular arrangements observed in the STM experiment. The configuration of the first three structures that form for increasing coverage is the same both experimentally and theoretically. In all three structures, the molecules only occupy the fcc and hcp adsorption sites. Yet, at high coverage, at which the top adsorption sites become occupied, a discrepancy arises

Cadherin-11 is expressed in detrusor smooth muscle cells and myofibroblasts of normal human bladder.

Contains fulltext : 52944schalken.pdf (publisher's version ) (Closed access)OBJECTIVES: It has recently been found that detrusor smooth muscle cells and myofibroblasts are coupled via gap junctions. However, gap junctions cannot account for strong physical interaction between cells, which has prompted the search for intercellular adhesion molecules. Cadherin-11 is a candidate for such a molecule, since it mediates the interaction of dermal myofibroblasts in contractile wound granulation tissue. We therefore hypothesised that the physical adhesion between detrusor smooth muscle cells and myofibroblasts is mediated by cadherin-11. The aim of this study was to test this hypothesis. METHODS: Bladder biopsies from eight radical cystectomy specimens were snap-frozen, sectioned, and stained for E-cadherin; cadherin-11; alpha-catenin; beta-catenin; gamma-catenin; and smooth muscle cell/myofibroblast markers connexin-43, vimentin, desmin, smooth muscle actin, and smoothelin. Specimens were analysed by using binocular epifluorescent and confocal laser-scanning microscopy. RESULTS: Specific positive membranous expression of all adhesion complex molecules except E-cadherin was detected in detrusor suburothelial tissue. All biopsies showed a similar punctate pattern of expression for cadherin-11 within bundles of smooth muscle cells and a suburothelial layer of cells. Cadherin-11 was specifically located at the cell membrane, in distinct linear domains. CONCLUSIONS: To our knowledge this is the first time evidence has been provided for cadherin-mediated smooth muscle and suburothelial myofibroblast cell-cell interaction in the human bladder. Cadherin-11 most probably plays an important role in the intercellular physical coupling of detrusor smooth muscle cells and also of myofibroblasts

Antigen expression of metastasizing and non-metastasizing human melanoma cells xenografted into nude mice

Contains fulltext : 27184___.PDF (publisher's version ) (Open Access

Improving the barrier function of damaged cultured urothelium using chondroitin sulfate

Item does not contain fulltextAIMS: To determine whether glycosaminoglycan (GAG) replenishment is able to improve recovery of a deficient urothelial barrier, chondroitin sulfate (CS) instillations were tested using an in vitro model. Porcine urothelial cells (Ucells) were terminally differentiated in culture conditions to construct a urothelial layer with a functional barrier. This layer was damaged to compromise barrier function to simulate a key characteristic of bladder pain syndrome/interstitial cystitis. The functional effect of subsequent treatment with CS was evaluated. METHODS: Primary porcine Ucells were isolated and cultured on inserts. Differentiation of cells was evaluated with immunohistochemical analysis for the presence of umbrella cells, tight junctions and CS. Transepithelial electrical resistance (TEER) measurements were performed to evaluate barrier function. Protamine was used to simulate mild urothelial damage. CS 0.2% (vol/vol), a GAG, was subsequently instilled in the treatment group. The recovery of barrier function was further evaluated with TEER measurements. The Student t test was used for the analysis of results. RESULTS: After induction of differentiation, the Ucells expressed barrier markers and a functional barrier was established (measured by high TEER). TEER decreased significantly after instillation with protamine. CS instillation improved recovery of TEER significantly measured after 7 hours (84% vs 22% in controls). After 24 hours; however, the TEER was comparable in both experimental groups. CONCLUSION: CS instillation improves the recovery of the urothelial barrier after damage in vitro. This functional experiment shows that CS improves recovery of damaged urothelial function, which supports the hypothesis behind the mechanism of action of GAG-replenishment therapy