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Vitamin titers

In nature, vitamin A aldehyde is produced by the oxidative cleavage of P-carotene by 15,15 - P-carotene dioxygenase. Alternatively, retinal is produced by oxidative cleavage of P-carotene to P-apo-S -carotenal followed by cleavage at the 15,15 -double bond to vitamin A aldehyde (47). Carotenoid biosynthesis and fermentation have been extensively studied both ia academic as well as ia iadustrial laboratories. On the commercial side, the focus of these iavestigations has been to iacrease fermentation titers by both classical and recombinant means. [Pg.101]

PCCs contain the vitamin K-dependent factors II, VII, IX, and X. These agents represent another attempt to bypass the factor at which the antibody is directed (see Fig. 64-2). However, PCCs carry the risk of serious thrombotic complications. Porcine factor VIII is most useful when the inhibitor titer is less than 50 BU (see Fig. 64-2 for dose and frequency). Owing to its similarity to human factor VIII, porcine factor VIII participates in the coagulation cascade. However, most inhibitors have very weak neutralizing activity against it. Porcine factor VIII is a third-line agent (only after factor Vila and a PCC have failed) owing to a 15% incidence of cross-reactivity.15... [Pg.991]

It must be recognized that the serum antibody level which is utilized as a measure of antibody response probably reflects an equilibrium between the rate of antibody synthesis and release from the sites of S3mthesis, on the one hand, and the rate of destruction of circulating antibody, on the other. A change in any one of these factors could obviously affect the content of circulating antibodies. Thus, a decreased antibody titer per se cannot be taken as unequivocal proof for an actual impairment of antibody s3mthesis. The effects of a vitamin deficiency upon antibody release and degradation must be evaluated before a definite relationship between vitamins and antibody synthesis can be established. [Pg.21]

The possible functions of pantothenic acid, pyridoxine, or folic acid in the mechanisms involved in the release of antibody from their sites of formation were further investigated as follows (Ludovici et al., 1951b). Rats were immunized with human erythrocytes while on the deficient diets and their initial titers determined. Four days later the animals were injected intraperitoneally with the respective vitamin and maintained on an adequate control diet for the remainder of the experiment. Antibody titers were determined periodically thereafter. The effect of the... [Pg.21]

Studies Serum IgM anti-GMl antibody titers were elevated. Serum blood counts, general chemistries, vitamin levels, and thyroid and parathyroid tests were normal. CSF protein was 68 mg/dL (normal up to 45 mg/dL). Nerve conductions showed an asymmetric dysschwannian motor polyneuropathy, with "conduction blocks" involving his upper more than... [Pg.65]

Figure 1, Hemagglutination Titer (7 Days) in Chicks Immunized Against Sheep Red Blood Cells. Vitamin E Supplement 300 mg/kg Diet as [dl]-a-tocopheryl Acetate,... Figure 1, Hemagglutination Titer (7 Days) in Chicks Immunized Against Sheep Red Blood Cells. Vitamin E Supplement 300 mg/kg Diet as [dl]-a-tocopheryl Acetate,...
An example is the immunoenhancement of mice against SRBC by vitamin E versus the synthetic antioxidant DPPD (N,N-rdiphenyl-p-phenylene diamine), shown in Table III. It is clear that DPPD was not as effective an immunoenhancer as vitamin E, particularly in causing the early IgM to IgG shift. (The HA titer after 2-mercapto-ethanol[2-ME] reduction is indicative of IgG), It is particularly interesting that mice on the vitamin E deficient diet had a very low PFC response and no IgG response. DPPD supplemented at twice the level used by others for reversing some vitamin E... [Pg.32]

In vitamin E and vitamin A interaction a synergism may be expected, due to the well documented sparing effect of vitamin E on vitamin A (Bauernfiend, Newmark and Brin, 1974). To our surprise we have found an antagonistic effect in chicks infected with E, coli (Tengerdy and Brown, 1977 Tengerdy and Nockels, 1974). This is shown in Table VI. The antagonistic effect was evident in mortality and HA titers but not in blood clearance of E, coli (phagocytosis). [Pg.39]


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See also in sourсe #XX -- [ Pg.27 , Pg.28 ]




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