Control of the Compound Zone or White Layer

2003 ◽  
pp. 65-70

Abstract The compound zone is more commonly known as the white layer, simply because when the nitrided sample is sectioned through the case, and then polished and etched with a standard solution of nital (2 to 5% nitric acid and alcohol), the immediate surface etches out white in appearance above the nitrided case. This chapter focuses on the methods to control the compound zone or white layer. It first provides information on a test to determine the presence of the white layer, and discusses the processes involved in the reduction of the compound zone by the two-stage process. Next, it describes the methods for controlling compound zone formation, and, finally, reviews the factors related to the determination of case depth nitriding.

2019 ◽  
Vol 70 (2) ◽  
pp. 242-262
Author(s):  
David Gibbs-Kneller ◽  
Derek Whayman

The determination of the scope of the fiduciary duty of loyalty, when created by contract, is not a unitary process. It is raised following a multi-factorial enquiry, which considers the nature of the engagement, in a first stage. Here, no single factor is conclusive. It is then, in a separate, second stage, reduced by qualifying contractual terms, which are applied almost strictly logically. This second stage uses the contractual doctrines of interpretation and implication. However, since it is a form of the fiduciary doctrine of authorisation, those contractual doctrines are modified according to fiduciary principles. We argue this follows from the underlying nature of the fiduciary obligation as a way of resolving its internal tensions. While this division has not yet been fully recognised in the cases, the courts have been inching towards it. However, not fully recognising this inevitable division and eliding the two stages has led to defective reasoning and outcomes.


2003 ◽  
pp. 31-37

Abstract Formation of the nitrided case begins through a series of nucleated growth areas on the steel surface. These nucleating growth areas will eventually become what is known as the compound layer or, more commonly, the white layer. This chapter discusses the influence of carbon on the compound zone. It explains how to control and calculate compound zone thickness. Compound zone thickness can be controlled by dilution, the two-stage Floe process, or by ion nitriding. The chapter describes the factors affecting surface case formation.


1970 ◽  
Vol 23 (02) ◽  
pp. 191-201 ◽  
Author(s):  
H. D Bruhn ◽  
L Müller ◽  
F Duckert

SummaryA modification of the caseinolytic assay for plasminogen is described. This assay system is characterized by the following features :1. Urokinase is used as activator achieving a complete activation of the plasminogen whereas with streptokinase caseinolytically inactive plasminogen-activator complexes are formed.2. All incubation times are reduced to the minimum which is still compatible with accuracy.3. Results are expressed in percent of a standard of ten normal plasmas.4. In this two-stage assay-system (activation of plasminogen to plasmin, digestion of casein by plasmin) both stages proceed simultaneously in the same system, thus the plasmin formed is stabilized “in statu nascendi” by the casein.5. Several conditions (stability of plasminogen in frozen plasma, use of anticoagulants, reproducibility) are defined.


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.


2017 ◽  
Vol 11 (8) ◽  
pp. 613
Author(s):  
Komang Astana Widi ◽  
Wardana Wardana ◽  
Wahyono Suprapto ◽  
Yudy Surya Irawan

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