California nurses unite to fight AIDS.
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
S N Davis
Publications and source records attributed to S N Davis.
Multiple myeloma as a cause of chylothorax.
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Aged↗
Regulation of ketogenesis, gluconeogenesis, and glycogen synthesis by insulin and proinsulin in rat hepatocyte monolayer cultures.
The metabolic actions of porcine insulin and biosynthetic human proinsulin on fatty acid and glucose metabolism were studied in rat hepatocytes cultured in monolayer for 24 h. Our aim was to establish whether proinsulin action in the liver is similar to insulin action and whether the relative potencies of the two hormones are the same for different metabolic processes. Proinsulin and insulin exerted a similar maximal inhibitory effect on ketone body formation from palmitate and on gluconeogenesis from pyruvate. The half-maximal effective concentration of proinsulin was 11-13 times that of insulin. The antiketogenic effects of insulin and proinsulin were associated with an increased glycerol 3-phosphate content and a decreased affinity of carnitine palmitoyltransferase for its substrate palmitoyl-CoA. When the basal rate of ketogenesis was increased with isobutyl methylxanthine, the half-maximal effective concentrations of both proinsulin and insulin were decreased, but the relative potency of the two hormones was unchanged. Proinsulin and insulin exerted similar maximal stimulatory effects on glycogen synthesis and on the activities of pyruvate kinase, glucose 6-phosphate dehydrogenase, phosphogluconate dehydrogenase, and malic enzyme. The half-maximal effective concentration of proinsulin was 10-30 times that of insulin. These findings are consistent with receptor binding studies on liver membranes that suggest that proinsulin interacts with insulin-specific and not proinsulin-specific receptors. Our findings also suggest that proinsulin action does not differ from insulin action at a postreceptor site.
Animals↗
Prolonged ventilation in acute severe asthma caused by the Guillain-Barre-Strohl syndrome.
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Acute Disease↗
Guidelines for nonemergency use of parenteral phenytoin products: proceedings of an expert panel consensus process. Panel on Nonemergency Use of Parenteral Phenytoin Products.
This document summarizes the proceedings of an expert panel consensus process addressing the nonemergency use of parenteral phenytoin products for management of seizures in pediatric and adult patients. The algorithm and consensus statements developed by the expert panel emphasize strategies for lowering the probability of adverse events associated with the use of parenteral phenytoin products. Specific patient characteristics are defined to guide administration and monitoring of parenteral phenytoin therapy. The algorithm provides a decision pathway for the selection of the product and the route of administration of phenytoin sodium or fosphenytoin sodium after it has been determined that a parenteral phenytoin product is appropriate. Key factors covered in the algorithm include a list of patient characteristics and considerations necessary to prevent parenteral phenytoin adverse effects during selection of administration route and recommendations for monitoring of parenteral phenytoin therapy once it has been initiated. Situations requiring rapid attainment of high phenytoin concentrations, such as in the management of acute seizures, are not addressed in these guidelines.
Adolescent↗
Evidence for a vicious cycle of exercise and hypoglycemia in type 1 diabetes mellitus.
Exercise is a cornerstone of diabetes management as it aids in glycemic control, weight management, reducing blood pressure, and improving the quality of life of patients. Unfortunately, owing to the complexity and difficulties of regulating exogenous insulin in a physiologic manner during exercise, physical activity often results in hypoglycemia in patients with type 1 diabetes mellitus (type 1 DM). When glucose levels fall below threshold glycemic levels, neuroendocrine, autonomic nervous system (ANS), and metabolic glucose counterregulatory mechanisms are activated. These hypoglycemic counterregulatory mechanisms in type 1 DM can be blunted irreversibly by disease duration or by acute episodes of prior stress. These reduced (or absent) counterregulatory responses result in a threefold increase in severe hypoglycemia when intensive glycemic control is implemented in type 1 DM. Much recent work has been focused on determining the in vivo mechanisms responsible for causing the increased incidence of severe hypoglycemia in type 1 DM. Studies from several laboratories have demonstrated the role played by episodes of antecedent hypoglycemia in producing blunted glucose counterregulatory responses during subsequent exposures of hypoglycemia. Until recently, the mechanisms responsible for exercise related hypoglycemia in type 1 DM have been attributed to relative or absolute increases of insulin levels or incomplete glycogen repletion after physical activity. Owing to the qualitative similarity of neuroendocrine, ANS, and metabolic responses to hypoglycemia and exercise, we have hypothesized that neuroendocrine and ANS counterregulatory dysfunction may also play an important role in the pathogenesis of exercise-related hypoglycemia in type 1 DM. Vicious cycles can be created in type 1 DM, where an episode of hypoglycemia or exercise can feed forward to downregulate neuroendocrine and ANS responses to a subsequent episode of either stress, thereby creating further hypoglycemia. This article will review the recent work that has studied the contribution of counterregulatory dysfunction to exercise-induced hypoglycemia in type 1 DM.
Blood Glucose↗
The effects of HDV-insulin on carbohydrate metabolism in Type 1 diabetic patients.
The aim of this study was to compare the metabolic effects of a single equimolar subcutaneous injection of hepatic directed vesicle-insulin (HDV-insulin) and regular insulin on glucose levels and intermediary metabolism during a 75-g oral glucose tolerance test (OGTT). Nine Type 1 diabetic patients underwent two experiments separated by 4 weeks. Each experimental protocol consisted of an identical evening meal followed by overnight euglycemic control achieved by a continuous low-dose insulin infusion. The next morning a subcutaneous injection (0.1 U/kg) of HDV-insulin or regular insulin was administered 30 min before a 75-g OGTT. The overnight basal insulin infusion was maintained unaltered throughout the 150-min OGTT. Plasma glucose, glucoregulatory hormones (insulin, glucagon, cortisol), and intermediary metabolites (lactate, alanine, glycerol, NEFA, beta-hydroxybutyrate) were measured to assess the metabolic effects of the two insulin preparations. Compared to regular insulin, an equivalent subcutaneous dose of HDV-insulin significantly lowered glucose levels during OGTT (mean reduction 2.2+/-0.4 mmol/l; P<.005). Plasma levels of insulin and glucagon were equivalent during both series of experiments. Blood lactate, glycerol and plasma NEFA levels were not different during OGTT indicating similar peripheral action of the insulins. beta-Hydroxybutyrate levels were significantly reduced (P<.05) following HDV-insulin supporting a preferential hepatic action of the preparation. We conclude that HDV-insulin can significantly lower plasma glucose excursions compared to an equivalent dose of regular insulin during an OGTT in Type 1 diabetic patients. The metabolic profile of equivalent peripheral insulin, glucagon and glycerol levels but reduced beta-hydroxybutyrate values support a hepatospecific effect of HDV-insulin.
Adult↗