Role of surfactants in the control of dopamine–eumelanin particle size and in the inhibition of film deposition at solid–liquid interfaces

In a liquid-STM setup environment, the redox behavior of manganese porphyrins was studied at various solid–liquid interfaces. In the presence of a solution of Mn(III)Cl porphyrins in 1-phenyloctane, which was placed at a conductive surface, large and constant additional currents relative to a set tunneling current were observed, which varied with the magnitude of the applied bias voltage. These currents occurred regardless of the type of surface (HOPG or Au(111)) or tip material (PtIr, Au or W). The additional currents were ascribed to the occurrence of redox reactions in which chloride is oxidized to chlorine and the Mn(III) center of the porphyrin moiety is reduced to Mn(II). The resulting Mn(II) porphyrin products were identified by UV–vis analysis of the liquid phase. For solutions of Mn(III) porphyrins with non-redox active acetate instead of chloride axial ligands, the currents remained absent.

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Overview

Introduction to Scanning Tunneling Microscopy ◽

10.1093/oso/9780198856559.003.0001 ◽

2021 ◽

pp. 1-40

Author(s):

C. Julian Chen

Keyword(s):

Elementary Theory ◽

Atomic Resolution ◽

Tunneling Conductance ◽

Liquid Interfaces ◽

Covalent Bonds ◽

Atom Manipulation ◽

The One ◽

Atomic States ◽

Solid Liquid

This chapter presents the basic designs and working principles of STM and AFM, as well as an elementary theory of tunneling and the imaging mechanism of atomic resolution. Three elementary theories of tunneling are presented: the one-dimensional Schrödinger’s equation in vacuum, the semi-classical approximation, and the Landauer formalism. The relation between the decay constant and the work function, and a general expression of tunneling conductance versus tip-sample distance are derived. A brief summary of experimental facts on the mechanism of atomic resolution STM and AFM is presented, which leads to a picture of interplay between the atomic states of the tip and the sample, as well as the role of partial covalent bonds formed between those electronic states. Four illustrative applications are presented, including imaging self-assembed molecules on solid-liquid interfaces, electrochemical STM, catalysis research, and atom manipulation.

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In-Situ Scanning Probe Microscopy of Solid-Liquid Interfaces: Role of Epitaxial Oxide Adlayers on Cu Electrodeposition

MRS Proceedings ◽

10.1557/proc-355-247 ◽

1994 ◽

Vol 355 ◽

Author(s):

John R. LaGraff ◽

Andrew A. Gewirth

Keyword(s):

Scanning Probe Microscopy ◽

Scanning Probe ◽

Liquid Interfaces ◽

Probe Microscopy ◽

Solid Liquid ◽

Epitaxial Oxide

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Fibrin Formation: The Role of the Fibrinogen-Fibrin Monomer Complex

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648007 ◽

1976 ◽

Vol 36 (01) ◽

pp. 037-048 ◽

Cited By ~ 49

Author(s):

Eric P. Brass ◽

Walter B. Forman ◽

Robert V. Edwards ◽

Olgierd Lindan

Keyword(s):

Particle Size ◽

Induction Period ◽

Fibrin Clot ◽

Clot Formation ◽

Appreciable Amount ◽

Buffer System ◽

Homeostatic Mechanism ◽

Fibrin Formation ◽

Fibrin Monomer

SummaryThe process of fibrin formation using highly purified fibrinogen and thrombin was studied using laser fluctuation spectroscopy, a method that rapidly determines particle size in a solution. Two periods in fibrin clot formation were noted: an induction period during which no fibrin polymerization occurred and a period of rapid increase in particle size. Direct measurement of fibrin monomer polymerization and fibrinopeptide release showed no evidence of an induction period. These observations were best explained by a kinetic model for fibrin clot formation incorporating a reversible fibrinogen-fibrin monomer complex. In this model, the complex serves as a buffer system during the earliest phase of fibrin formation. This prevents the accumulation of free polymerizable fibrin monomer until an appreciable amount of fibrinogen has reacted with thrombin, at which point the fibrin monomer level rises rapidly and polymerization proceeds. Clinically, the complex may be a homeostatic mechanism preventing pathological clotting during periods of elevated fibrinogen.

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