Albumin critical values

Based on associations between abnormal serum J32m, -globulin and urinary albumin values and the number of times the PbB was above critical values, Chia et al. (1995a) suggested that the threshold of 70 pg/dL for PbB may not prevent the occurrence of nephropathy. 

Whole serum does not bind phenol red below a critical albumin concentration of 1.6 g%. Above this critical value, dye is bound in direct proportion to the amount of albumin in excess of the critical value. In jaundice the critical value is elevated. These results were taken to indicate that some binding sites in whole serum are occupied by, for example, bilirubin, bile acids, or fatty acids (B27). Bile salts reduce the binding of BSP (All, A14, R18a). This effect may be due to the detergent properties of bile salts because Teepol has been found to have a similar effect (A14). Binding of rose bengal was not affected by sodium dehydro-cholate or by BSP (E4). 

The amide I region for hot pressed films of egg albumin, lactalbumin, feather keratin and wheat gluten were analysed with deconvolution software. Increased order was observed in the form of p-sheets as glycerol content increased up to a critical value for each protein. Beyond this, critical value order decreased." The result of the deconvolution for wheat gluten is summarized in Figure 7.18. 

The introduced THEOS did not bring about precipitation in protein solutions. This behavior differs from that observed with common silica precursors. For example, TEOS added in such small amounts caused precipitation. By using THEOS, we could prepare homogeneous mixtures. When its amount introduced into the albumin solution was less than 5 wt.%, there was no transition to a gel state (Table 3.1). A gradual increase in THEOS concentration resulted in a rise in the solution viscosity. The transition to a gel state took place as soon as a critical concentration was reached. Its value, as demonstrated in Ref. 

Reduction in colloidosmotic pressure The colloidosmotic pressure in the plasma is lower in hver cirrhosis patients. This results from (1.) restriction in the synthesis of albumin (which is, however, only clinicaUy manifest after 3 or 4 weeks due to the half-life of plasma albumin), (2.) greater loss of protein-rich fluid in the abdominal cavity, and (3.) dilution of the vascular volume. A critical concentration of albumin in the plasma is deemed to be about 3 g/100 ml (ca. 435 pmol/1). Below this albumin value, there is a clear correlation between portal hypertension and the formation of ascites. The coexistence of portal hypertension and hypalbuminaemia (critical concentration 2.5—3.0 gldl) is an important prerequisite for the formation of ascites. 

An important consideration is, which results should be reported when ICa " "], pH, and the calculated [Ca " "] at pH 7.4 are all produced by the instrument. The algorithms used to calculate the latter variable assume normal concentrations of total protein and albumin, normal binding of Ca " " to plasma proteins, and a standard Ap[Ca ]/ApH ratio of 0.23 for all patients [23]. Use of these algorithms also assumes that in vivo and in vitro pH changes have equivalent effects on Ca and that respiratory and metabolic acid-base disorders produce equivalent changes in Ca [23]. Since these assumptions probably oversimplify the complex equilibria between species, particularly in critically ill patients, it is generally agreed that only the measured Ca and the pH values should be reported. 

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