Cardiac antibody production to self-antigens in children and adolescents during and following the correction of severe diabetic ketoacidosis.

Diabetic cardiomyopathy (DC) is an independent phenotype of diabetic cardiovascular disease. The understanding of the pathogenesis of DC in young patients with type 1 diabetes (T1D) is limited. The cardiac insults of diabetic ketoacidosis (DKA) and progression of DC could include development of antibodies (Abs) to cardiac self-antigens (SAgs) such as: myosin (M), vimentin (V) and k-alpha 1 tubulin (Kα1T).

Increased systemic Th17 cytokines are associated with diastolic dysfunction in children and adolescents with diabetic ketoacidosis.

Diastolic dysfunction suggestive of diabetic cardiomyopathy is established in children with T1DM, but its pathogenesis is not well understood. We studied the relationships of systemic inflammatory cytokines/chemokines and cardiac function in 17 children with T1DM during and after correction of diabetic ketoacidosis (DKA). Twenty seven of the 39 measured cytokines/chemokines were elevated at 6-12 hours into treatment of DKA compared to values after DKA resolution.

Empirical evidence of the effectiveness of concept mapping as a learning intervention for nuclear medicine technology students in a distance learning radiation protection and biology course.

Unlabelled: Metacognitive learning strategies are based on instructional learning theory, which promotes deep, meaningful learning. Educators in a baccalaureate-level nuclear medicine technology program demonstrated that students enrolled in an online, distance learning section of an introductory radiation protection and radiobiology course performed better when traditional instruction was supplemented with nontraditional metacognitive learning strategies.

Methods: The metacognitive learning strategy that was used is best known as concept mapping.

Development of a concept map to convey understanding of patient and family-centered care.

Even though the expression "Patient and Family-Centered Care (PFCC)" is widely used, there remains a lack of clarity regarding how the fundamental tenets of PFCC fit with our current model of healthcare. The purpose of this manuscript was to describe the first step in developing an organizational understanding of the operational construct for PFCC utilizing a concept map and the fundamental concept mapping learning theories. The overall goals were to build a more robust organization-wide understanding of the basic PFCC tenets guided by the philosophy of concept mapping.

Insulin and IGF-1 receptors, nitrotyrosin and cerebral neuronal deficits in two young patients with diabetic ketoacidosis and fatal brain edema.

Gray and white matter structural deficits may accompany type 1 diabetes. Earlier experimental studies have demonstrated neuronal deficits associated with impaired neurotrophic support, inflammation and oxidative stress. In this study we demonstrate in two patients with histories of poorly controlled type 1 diabetes and fatal brain edema of ketoacidosis neuronal deficits associated with a decreased presence of insulin and IGF-1 receptors and accumulation of nitrotyrosin in neurons of affected areas and the choroid plexus.

Receptor for advanced glycation end products and neuronal deficit in the fatal brain edema of diabetic ketoacidosis.

Radiologic and neuropsychologic studies suggest that diabetes mellitus causes structural changes in the brain and adversely effects cognitive development. Experimental animal models of type 1 diabetes mellitus (T1DM) have advanced these findings by demonstrating duration-related neuronal and cognitive deficits in T1DM BB/Wor rats. We studied the expression of receptor for advanced glycation end products (RAGE) and neuronal densities in the brains of two patients who died as the result of clinical brain edema(BE)that developed during the treatment of severe diabetic ketoacidosis (DKA).

Study of subclinical cerebral edema in diabetic ketoacidosis by magnetic resonance imaging T2 relaxometry and apparent diffusion coefficient maps.

Cerebral edema is the most significant complication in children with diabetic ketoacidosis (DKA). Our goal was to study whether subclinical cerebral edema was preferentially vasogenic or cytotoxic. Magnetic resonance imaging (MRI)--diffusion-weighted imaging (DWI) and T2 relaxometry (T2R)--were obtained in pediatric patients presenting with severe diabetic ketoacidosis (DKA) 6-12 hours after initial DKA treatment and stabilization and 96 hours after correction of DKA.

Diabetic ketoacidosis increases extracellular levels of the major inducible 70-kDa heat shock protein.

Objectives: Diabetic ketoacidosis (DKA) represents a metabolic stress whose treatment induces a systemic proinflammatory cytokine profile and accentuates life-threatening acute complications. The present study determined whether serum levels of the major inducible 70-kDa heat shock protein (Hsp72), a modulator of cytokine expression, were influenced by DKA and its treatment.

Design And Methods: Serum levels of Hsp72 and glucose were measured in five adolescents with type 1 diabetes mellitus (T1DM) prior to, during and following correction of severe DKA.

Retinal vascular integrity following correction of diabetic ketoacidosis in children and adolescents.

Objective: Increased permeability of the cerebral microvasculature occurs during the treatment of diabetic ketoacidosis (DKA). Microvascular changes consistent with diabetic retinopathy have been reported prior to and after the treatment of DKA. This study evaluated the structural and functional aspects of the retina immediately following the correction of DKA.

Complement activation in diabetic ketoacidosis and its treatment.

Recent studies support the presence of an inflammatory response during the treatment of diabetic ketoacidosis (DKA). The objectives of this study were to monitor the complement activation products C3a, C4a, Bb, and C5b-9 prior to, during, and after correction of DKA. All patients had increased levels of C3a at 6-8 h and 24 h (P<0.

Plasma C-reactive protein levels in severe diabetic ketoacidosis.

Elevated plasma levels of C-reactive protein (CRP) and IL-6 have been reported to be sensitive indicators of infection in adults with diabetic ketoacidosis (DKA). However, both CRP and the pro-inflammatory cytokines, which regulate CRP, can be elevated without infection. Our hypothesis was that CRP is increased in young patients with severe DKA, even in the absence of an infection, and may serve as a marker for systemic inflammatory response syndrome (SIRS).

Diabetic ketoacidosis and its treatment increase plasma 3-deoxyglucosone.

Objectives: Highly reactive dicarbonyl compounds are known to be increased by hyperglycemia, ketone bodies and lipid peroxidation. This study was carried out to investigate the effect of diabetic ketoacidosis (DKA) and its treatment on the plasma concentration of 3 deoxyglucosone (3-DG) one of the dicarbonyl compounds.

Design And Methods: 3-DG was measured in 7 children before, during and following correction of severe DKA.

Diabetic ketoacidosis promotes a prothrombotic state.

Cerebrovascular accidents are one of the life-threatening complications of diabetic ketoacidosis (DKA) in children and adolescents. Our objective was to evaluate the effect of DKA and its treatment on factors known to affect thrombotic activity (protein C; protein S; von Willebrand factor, fibrinogen; homocysteine; and folate) by comparing seven adolescents with DKA prior to treatment and at 6, 24, and 120 hours after initiation of treatment. We found that protein C activity was significantly decreased by DKA, but normalized slowly following treatment.

Acetoacetate increases expression of intercellular adhesion molecule-1 (ICAM-1) in human brain microvascular endothelial cells.

It has been hypothesized that ketone bodies cause activation of brain endothelial cells and that this is a factor in the intracerebral crises of diabetic ketoacidosis (DKA). In this study we used cultured human brain microvascular endothelial cells (HBMEC) to investigate the effect of beta hydroxybutyrate (BOHB) and acetoacetate (AcAc) on the expression of the adhesion molecule, intercellular adhesion molecule-1 (ICAM-1). Increasing concentrations of AcAc, but not BOHB, caused a significant upregulation of ICAM-1 in comparison to unstimulated cells.