Who understands what you do?
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Biomedical subjects
Publications and source records attributed to T A Sherwood.
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Managed care, in addition to being driven by the hegemony of market concerns, has truly bitten into the clinical hegemony. Nursing has recognized this new order and is attempting to manage the situation with new paradigms before other non-nursing entities do. The issue for nursing has become how to allow the patient to drive the health care delivery system while preparing for change and not fearing nursing's loss of preeminence as a clinical authority in its own right. At the same time, nursing must protect a valued and needed profession.
A direct LDL cholesterol assay was evaluated using immunoprecipitation (Sigma Diagnostics, St. Louis, MO) with beta-quantification obtained by ultracentrifugation. Excellent intra- and interassay coefficients of variation were obtained (< 4.5%). There was a good correlation (r = 0.88, P < .0001) between the two methods for low-density lipoprotein cholesterol (LDL-C) in 249 samples with triglyceride levels ranging from 13 mg/dL to 2,236 mg/dL and LDL cholesterol levels ranging from 28 mg/dL to 290 mg/dL. Similar correlations were seen for patients with triglyceride levels < 400 mg/dL (r = 0.89, n = 174) and > or = 400 mg/dL (r = 0.89, n = 75). However, using the Friedewald equation, there was a good correlation only in samples with triglyceride levels < 400 mg/dL. No significant differences were found between LDL-C quantitated by the direct LDL assay and beta quantification for patients with dysbetalipoproteinemia (Type III disorder). However, calculated LDL values using the Friedewald equation were found to be significantly higher when compared to beta-quantification in patients with the Type III disorder. There was a slight but significant decrease in LDL-C determined by direct LDL cholesterol assay for non-fasting versus fasting serum (4.7%) despite a strong correlation between these samples (r = 0.98, P < .0001). In addition, freezing samples for 30 days resulted in a significant decrease in levels (15.1%). Thus, this direct LDL cholesterol assay is recommended in place of beta-quantification in hypertriglyceridemic samples (TG > or = 400 mg/dL) and to monitor LDL cholesterol levels in patients with Type III dyslipidemia, because it is less time consuming, more cost-effective and can be adapted to the clinical laboratory.
White Leghorn hens were fed purified folate-deficient diets or commercial corn- and soybean meal-based diets supplemented with different amounts of folic acid. The folate contents of egg yolk and blood plasma from these hens were estimated with an isotope-dilution, radioligand-binding assay. Folates in egg yolk were concentrated approximately 43-fold relative to the blood plasma from which they were derived. Yolk and plasma folate concentrations became saturated with increasing dietary folate. Hens fed a commercial, folate-sufficient diet (0.72 mg folate/kg) produced eggs with slightly less than half of the maximal folate content. Based on tritium deposition in egg yolk and egg white, the biological half-life of [3H]folic acid injected intraperitoneally into two folate-sufficient hens was approximately 15 days, while it was > or = 40 days in two hens fed a purified folate-deficient diet (0.07 mg folate/kg) that also reduced egg production. Radioactivity in egg yolk was concentrated more than 100-fold relative to egg white in both cases. The [3H]folates remaining in the hens at the end of the experiment were substantially more concentrated in liver than in kidney, heart, or skeletal muscle. The specific radioactivity of folates in the liver of folate-deficient hens after 78 days was almost 10 times greater than in folate-sufficient hens after 39 days. Laying hens have highly efficient conservation and delivery systems for folates.
Normal chicken eggs contain substantial amounts of riboflavin, all of which is bound to a specific, high-affinity, riboflavin-binding protein (RfBP). Two hens, genetically unable to produce RfBP and thus unable to deposit sufficient riboflavin in their eggs, were compared to two normal hens with respect to the biological half-life of [14C]riboflavin, the tissue distribution of 14C-labeled flavins, and the relative contributions of tissue and dietary riboflavin to flavins deposited in the egg. The biological half-life of [14C]riboflavin was slightly but insignificantly less in the RfBP-deficient hens (11.5 +/- 1.7 days vs 15.1 +/- 3.3 days). The 14C-labeled flavin content of a variety of tissues 3 weeks after the intraperitoneal injection of 5 microCi of riboflavin was also very similar among the four hens. In contrast, the 14C-labeled flavin content of egg yolk, egg albumen, and blood plasma from RfBP-deficient birds was less than 10% of normal. For all hens, the specific radioactivity of flavins in yolk and albumen was similar to that in liver but less than that in heart. We conclude that riboflavin deposited in egg had equilibrated with the large hepatic flavin pool and was not derived preferentially from unlabeled dietary riboflavin. Other than the inability to deposit riboflavin in their eggs, hens of the mutant strain have normal riboflavin metabolism.
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Soluble immune complexes (IC) are known to bind to human red blood cells (HRBC). Most authors have attributed this binding to the interaction between IC-bound C3b and a red cell CR1 receptor, but contradictory data has been published concerning the ability of IC to bind to HRBC in the absence of complement. Using soluble tetanus toxoid-rabbit anti-tetanus toxoid (TT-ATT) IC, we have shown that binding through the CR1 receptor takes place when IC are formed at antibody excess, while IC formed at antigen excess do not require complement for erythrocyte binding. Once absorbed to HRBC, IC are recognized by CR1 and/or Fc receptors on phagocytic cells. This interaction is not associated with red cell engulfment, but using radiolabelled S. aureus protein A as a probe, we have demonstrated the transfer of IC from HRBC to phagocytic cells. Such transfer without red blood cell (RBC) damage agrees with the postulated role of RBC in the elimination of soluble IC from circulation. However, we have also demonstrated that the interaction between HRBC-IC and phagocytic cells is associated with the release of mediators of inflammation. It is, therefore, not absolutely clear whether the interaction of RBC-adsorbed IC and phagocytic cells will always have beneficial consequences.
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