DETERMINATION OF COMPLEX SURFACE STRUCTURES WITH LEED

1997 ◽  
Vol 04 (03) ◽  
pp. 479-487 ◽  
Author(s):  
M. A. VAN HOVE

The evolution of the complexity of structural determination attainable with LEED is reviewed. Considerable progress in methodologies and computers has enabled structures as complex as Cu(100) + (4 × 4)- 10Li to be solved in terms of 18 fit parameters. The Si(111)-(7 × 7) structure could now be refined in terms of 100-or-so fit parameters, if a large-enough experimental dataset were available. Big challenges remain: finding a direct or quick way to identify the one qualitatively correct structure; and, to a lesser degree, providing the required size of the experimental dataset.

1993 ◽  
Vol 287-288 ◽  
pp. 428-431 ◽  
Author(s):  
M.A. Van Hove ◽  
W. Moritz ◽  
H. Over ◽  
P.J. Rous ◽  
A. Wander ◽  
...  

1993 ◽  
Vol 287-288 ◽  
pp. A394
Author(s):  
M.A. Van Hove ◽  
W. Moritz ◽  
H. Over ◽  
P.J. Rous ◽  
A. Wander ◽  
...  

1997 ◽  
Vol 04 (06) ◽  
pp. 1221-1226 ◽  
Author(s):  
SEIGI MIZUNO ◽  
HONG JIANG ◽  
HIROSHI TOCHIHARA

With increasing Li coverage on Cu(110), (n×1)(4≤n≤8) structures follow the (1×2) missing-row structure at room temperature. We determine the (4×1) structure by a dynamical low-energy electron diffraction (LEED) analysis with symmetrized automated tensor LEED. This completes the solution of the complex surface structures formed on low-index planes of copper single crystal by Li deposition. Every fourth Cu row in the [001] direction is substituted by Li atoms and the remaining Cu rows are covered by Li adatoms. Features of this structure, denoted as Cu (110)-(4×1)-3 Li , are very similar to those of the previously determined Cu (001)-(3×3)-5 Li , Cu (001)-(4×4)-10 Li and Cu (111)-(2×2)-3 Li structures.


1993 ◽  
Vol 19 (3-6) ◽  
pp. 191-229 ◽  
Author(s):  
M.A. Van Hove ◽  
W. Moritz ◽  
H. Over ◽  
P.J. Rous ◽  
A. Wander ◽  
...  

Author(s):  
R. L. Hines

The importance of atom layer terraces or steps on platinum surfaces used for catalysis as discussed by Somorjai justifies an extensive investigation of the structure of platinum surfaces through electron microscopy at the atomic resolution level. Experimental and theoretical difficulties complicate the quantitative determination of platinum surface structures but qualitative observation of surface structures on platinum crystals is now possible with good experimental facilities.Ultrathin platinum crystals with nominal 111 orientation are prepared using the procedure reported by Hines without the application of a carbon backing layer. Platinum films with thicknesses of about ten atom layers are strong enough so that they can be mounted on grids to provide ultrathin platinum crystals for examination of surface structure. Crystals as thin as possible are desired to minimize the theoretical difficulties in analyzing image contrast to determine structure. With the current preparation procedures the crystals frequently cover complete openings on a 400 mesh grid.


1967 ◽  
Vol 18 (01/02) ◽  
pp. 198-210 ◽  
Author(s):  
Ronald S Reno ◽  
Walter H Seegers

SummaryA two-stage assay procedure was developed for the determination of the autoprothrombin C titre which can be developed from prothrombin or autoprothrombin III containing solutions. The proenzyme is activated by Russell’s viper venom and the autoprothrombin C activity that appears is measured by its ability to shorten the partial thromboplastin time of bovine plasma.Using the assay, the autoprothrombin C titre was determined in the plasma of several species, as well as the percentage of it remaining in the serum from blood clotted in glass test tubes. Much autoprothrombin III remains in human serum. With sufficient thromboplastin it was completely utilized. Plasma from selected patients with coagulation disorders was assayed and only Stuart plasma was abnormal. In so-called factor VII, IX, and P.T.A. deficiency the autoprothrombin C titre and thrombin titre that could be developed was normal. In one case (prethrombin irregularity) practically no thrombin titre developed but the amount of autoprothrombin C which generated was in the normal range.Dogs were treated with Dicumarol and the autoprothrombin C titre that could be developed from their plasmas decreased until only traces could be detected. This coincided with a lowering of the thrombin titre that could be developed and a prolongation of the one-stage prothrombin time. While the Dicumarol was acting, the dogs were given an infusion of purified bovine prothrombin and the levels of autoprothrombin C, thrombin and one-stage prothrombin time were followed for several hours. The tests became normal immediately after the infusion and then went back to preinfusion levels over a period of 24 hrs.In other dogs the effect of Dicumarol was reversed by giving vitamin K1 intravenously. The effect of the vitamin was noticed as early as 20 min after administration.In response to vitamin K the most pronounced increase was with that portion of the prothrombin molecule which yields thrombin. The proportion of that protein with respect to the precursor of autoprothrombin C increased during the first hour and then started to go down and after 3 hrs was equal to the proportion normally found in plasma.


1969 ◽  
Vol 61 (2) ◽  
pp. 219-231 ◽  
Author(s):  
V. H. Asfeldt

ABSTRACT This is an investigation of the practical clinical value of the one mg dexamethasone suppression test of Nugent et al. (1963). The results, evaluated from the decrease in fluorimetrically determined plasma corticosteroids in normal subjects, as well as in cases of exogenous obesity, hirsutism and in Cushing's syndrome, confirm the findings reported in previous studies. Plasma corticosteroid reduction after one mg of dexamethasone in cases of stable diabetes was not significantly different from that observed in control subjects, but in one third of the insulin-treated diabetics only a partial response was observed, indicating a slight hypercorticism in these patients. An insufficient decrease in plasma corticosteroids was observed in certain other conditions (anorexia nervosa, pituitary adenoma, patients receiving contraceptive or anticonvulsive treatment) with no hypercorticism. The physiological significance of these findings is discussed. It is concluded that the test, together with a determination of the basal urinary 17-ketogenic steroid excretion, is suitable as the first diagnostic test in patients in whom Cushing's syndrome is suspected. In cases of insufficient suppression of plasma corticosteroids, further studies, including the suppression test of Liddle (1960), must be carried out.


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