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Nicole Glaser

Publications and source records attributed to Nicole Glaser.

12 recordsLinked to original sources
PubMed2006

Janus particles at liquid-liquid interfaces.

Following recent theoretical predictions, we report on the first experiments on the interfacial activity of so-called Janus nanoparticles (i.e., bifacial particles consisting of a gold and an iron oxide moiety). Using pendant drop tensiometry, we show that the amphiphilicity derived from the Janus character of the particles leads to a significantly higher interfacial activity compared to that of the respective homogeneous particles of the same size. The self-assembly of Janus particles at the hexane-water interface results in a significant decrease in the interfacial tension. Furthermore, we demonstrate control over the interfacial activity by tuning the particles' amphiphilicity via ligand-exchange reactions.

Journal Article↗
PubMed2006

Increased monocytic activity and biomarkers of inflammation in patients with type 1 diabetes.

Type 1 diabetes is associated with increased vascular complications, and monocytes are pivotal cells in atherogenesis. However, there are few data on monocyte function and inflammation in type 1 diabetes. The aim of this study was to compare monocyte function and biomarkers of inflammation in type 1 diabetic subjects without macrovascular disease with that in matched control subjects (n = 52 per group). Fasting blood was obtained for biomarkers of inflammation (C-reactive protein [CRP], plasma-soluble cell adhesion molecules [CAMs], monocyte chemoattractant protein 1, nitrotyrosine, CD40 ligand [CD40L], and monocyte function). High-sensitive CRP, soluble intracellular adhesion molecule (sICAM), sCD40L, and nitrotyrosine levels were significantly elevated in type 1 diabetic subjects compared with in control subjects (P < 0.05). Monocyte superoxide anion release was significantly increased in the resting (37%; P < 0.05) and activated state (26%; P < 0.005) in type 1 diabetic compared with in control subjects. Monocyte interleukin (IL)-6 levels were significantly elevated in type 1 diabetic subjects compared with in control subjects in the resting state (51%; P < 0.05) and after lipopolysaccharide activation (31%; P < 0.01). Monocyte IL-1beta levels were increased in the activated monocytes in type 1 diabetic compared with in control subjects. There were no significant differences in monocyte tumor necrosis factor levels or adhesion between the two groups. Thus type 1 diabetes is a proinflammatory state, as evidenced by increased levels of monocyte IL-6, superoxide anion, and plasma CRP, sICAM, sCD40L, and nitrotyrosine levels. These results have a major implication on our understanding of the role of inflammation in vasculopathies in type 1 diabetes.

Adult↗
PubMed2006

New perspectives on the pathogenesis of cerebral edema complicating diabetic ketoacidosis in children.

Cerebral edema is a serious complication of diabetic ketoacidosis (DKA) in children and is the most frequent diabetes-related cause of death in this age group. Many theories have been proposed to explain the pathogenesis of this complication, but data from the literature have not clearly supported any particular theory and DKA-related cerebral edema remains poorly understood. The question of whether DKA treatment may play a role in causing or exacerbating cerebral edema has been particularly controversial. Recent data have provided helpful evidence in favor or against various theories of pathogenesis and these data are the topic of the current review.

Brain Edema↗
PubMed2005

Administration of Lispro insulin with meals improves glycemic control, increases circulating leptin, and suppresses ghrelin, compared with regular/NPH insulin in female patients with type 1 diabetes.

CONTEXT: Overweight and obesity are overrepresented in adolescents with type 1 diabetes mellitus (T1DM). Exogenous insulin administration often poorly reproduces normal insulin patterns and may less effectively regulate leptin and ghrelin, two hormones involved in the control of appetite and adiposity. OBJECTIVE: The objective of the study was to determine whether insulin regimens that better replicate normal insulin patterns and augment postprandial nutrient disposal may help normalize leptin and ghrelin and improve body weight regulation. DESIGN, SETTING, AND PARTICIPANTS: Ten young women with T1DM were studied in this 2-wk prospective, balanced crossover-design study at the University of California, Davis. INTERVENTION: Participants received either a single injection of regular + NPH insulin (R+N) or two mealtime injections of Lispro insulin in randomized order on 2 separate days. Meal composition and total insulin administered were the same on both treatment days. MAIN OUTCOME MEASURES: Plasma glucose, insulin, leptin, and ghrelin concentrations were monitored over the 10-h study period. RESULTS: Lispro produced two distinct mealtime peaks of insulin, compared with one prolonged rise with R+N. Lispro reduced postprandial hyperglycemia and total glucose area under the curve. Leptin increased more on the Lispro (2.7 +/- 0.7 vs. 0.7 +/- 0.5 ng/ml, P = 0.02). Ghrelin was more suppressed after lunch with Lispro (P = 0.004). CONCLUSIONS: Injection of Lispro insulin with meals produces more physiological insulin patterns, better glucose control, and improved leptin and ghrelin regulation than R+N. More closely mimicking normal insulin, leptin, and ghrelin responses to meals with fast-acting insulin may have implications for body weight regulation in T1DM.

Adolescent↗
PubMed2005

Pediatric diabetic ketoacidosis and hyperglycemic hyperosmolar state.

Diabetic ketoacidosis is an important complication of diabetes in children and is the most frequent diabetes-related cause of death in childhood. The pathophysiology of this condition can be viewed as an exaggeration of the normal physiologic mechanisms responsible for maintaining an adequate fuel supply to the brain and other tissues during periods of fasting and physiologic stress. The optimal therapy has been a subject of controversy, particularly because the most frequent serious complication of diabetic ketoacidosis-cerebral edema-and the relationship of this complication to treatment are incompletely understood. In this article, the author reviews the pathophysiology of diabetic ketoacidosis and its complications and presents an evidence-based approach to the management of this condition.

Abdominal Pain↗
PubMed2005

Bumetanide reduces cerebral edema formation in rats with diabetic ketoacidosis.

The mechanisms responsible for cerebral edema formation in diabetic ketoacidosis (DKA) are not well understood, although evidence suggests ischemia as a contributing factor. Previous studies have shown that the Na-K-Cl cotransporter of cerebral microvascular endothelial cells and astrocytes is a major participant in ischemia-induced cerebral edema in stroke. The present study was conducted to test the hypothesis that the Na-K-Cl cotransporter also contributes to cerebral edema in DKA. Sprague-Dawley rats were administered streptozotocin to induce DKA, and then cerebral edema was assessed by determination of apparent diffusion coefficients (ADC) with magnetic resonance diffusion-weighted imaging. Cerebral ADC values in DKA rats were significantly reduced in both cortex and striatum compared with non-DKA control rats, indicating the presence of cerebral edema. Intravenous administration of bumetanide to DKA rats abolished the drop in cortical ADC values, while having no significant effect in the striatum. Insulin and saline treatment had no effect when given after bumetanide but increased both cortical and striatal ADC values when given before bumetanide. Evidence is also presented here that acetoacetate and beta-hydroxybutyrate stimulate brain microvascular Na-K-Cl cotransporter activity. These findings suggest that the Na-K-Cl cotransporter contributes to brain edema in DKA.

Animals↗
PubMed2005

Detection of cerebral {beta}-hydroxy butyrate, acetoacetate, and lactate on proton MR spectroscopy in children with diabetic ketoacidosis.

BACKGROUND AND PURPOSE: Ketone bodies provide important alternate fuel for brain metabolism, and their transport into the brain increases with prolonged fasting. During diabetic ketoacidosis (DKA), serum ketone concentrations markedly increase; however, little is known about whether ketone bodies accumulate in cerebral tissues during DKA. We used proton MR spectroscopy (MRS) to detect cerebral beta-hydroxy butyrate (betaOHB) and acetone/acetocaetate (AcAc) in children with DKA. METHODS: Twenty-five children underwent brain MRS: nine within 4 hours of the start of treatment for DKA; 11, at 4-8 hours; and five, at 8-12 hours. MRS was repeated after their recovery from the DKA episode at > or =72 hours after the start of treatment. MRS was evaluated for peaks corresponding to betaOHB (doublet centered on 1.20 ppm) and lactate (doublet centered on 1.33 ppm). Difference spectroscopy was used to identify the AcAc peak at 2.22-2.26 ppm. RESULTS: betaOHB was detected in 13 children (52%), more frequently within 4 hours (eight children, 89%) than after 4 hours (five children, 31%). AcAc was detected in 15 children (60%), more frequently at >4 hours after the start of treatment (12 patients, 75%) than in the first 4 hours (three patients, 33%). Lactate was detected in five children (18%), all within the first 8 hours of treatment. CONCLUSION: In children, betaOHB and AcAc accumulate in the brain during DKA, and they can be detected on MRS. Care should be taken in interpreting MRS results in patients with DKA to avoid erroneously attributing betaOHB peaks to lactate.

3-Hydroxybutyric Acid↗
PubMed2002

Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema.

OBJECTIVE: To investigate the relation between outcomes of children with diabetic ketoacidosis (DKA)-related cerebral edema and baseline clinical features and therapeutic interventions for treatment of cerebral edema. STUDY DESIGN: All children </=18 years old with DKA and cerebral edema (n = 61) were retrospectively identified from 10 pediatric centers between 1982 and 1997. Demographic, biochemical, and therapeutic data were collected. Ordinal logistic regression analysis was used to identify factors associated with the clinical outcome (death or persistent vegetative state; mild to moderate neurological disability; or normal) after adjusting for known risk factors for the development of cerebral edema as well as the degree of neurologic depression at the time of diagnosis of cerebral edema. RESULTS: Seventeen (28%) children died or survived in a vegetative state; 8 (13%) survived with mild to moderate neurologic disabilities; and 36 (59%) survived without sequelae. Factors associated with poor outcomes included greater neurologic depression at the time of diagnosis of cerebral edema, a high initial serum urea nitrogen concentration, and intubation with hyperventilation to a PCO (2) <22 mm Hg. CONCLUSIONS: After adjusting for potential confounding variables and the degree of neurologic compromise at the initiation of therapy, intubation with hyperventilation is associated with adverse outcomes of DKA-related cerebral edema. Greater neurologic depression at the time of diagnosis of cerebral edema and a higher initial serum urea nitrogen concentration are also associated with poor outcome.

Adolescent↗