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<p>Att drabbas av en kronisk sjukdom som diabetes påverkar vardagen för resten av livet. Allt fler barn drabbas av diabetes och som lärare innebär det att chansen att få möta dessa barn i skolan ökar. För barn i skolåldern kan sjukdomen påverka skolarbetet. Syftet med denna rapport är att undersöka hur diabetes påverkar inlärningsförmågan, samt undersöka vad en lärare behöver förstå angående barn med diabetes. Genom att intervjua en flicka med diabetes på mellanstadiet, hennes föräldrar och klassföreståndare har jag fått en personlig bild av hur det är att leva med diabetes i praktiken. De kan alla vittna om hur diabetes påverkar förmågan att koncentrera sig och att lära. Intervjuer med två diabetessköterskor visar att svaren från de andra respondenterna delvis kan tas för allmänna bland barn med diabetes. Denna rapport visar att diabetes har inverkan på inlärningsförmågan. Högt, lågt och svängande blodsocker gör diabetikern trött och okoncentrerad. Det är diabetikern själv, med hjälp av föräldrar och sjukvård, som ansvarar för att sjukdomen sköts på ett bra sätt. För läraren gäller det att ha en god förståelse för diabetessjukdomens påverkan på skolarbetet.</p> / <p>To suffer from a chronic disease such as diabetes affects everyday life for the rest of life. More and more children suffer from diabetes and the chances for teachers to meet one of these children in school are increasing. A child’s ability to perform at school can be affected by this disease. The purpose of this report is to investigate how diabetes affects the ability to learn and what a teacher must understand about children who have diabetes. I have learnt what it’s like to live with diabetes by interviewing a girl in middle school, her parents and her teacher. They can all testify about how diabetes affects the ability to focus and learn. Interviews with two nurses confirm that diabetes can have this effect on children. This report shows that diabetes affects the ability to learn. High, low and turning levels of blood sugar makes a diabetic tired and unfocused. The diabetic assisted by her parents and the medical treatment is responsible for handling the disease. The teacher however must understand how diabetes affects a child’s ability to perform at school.</p>

<p>Type 1 diabetes is a disease resulting from the progressive immune-mediated destruction of insulin producing β-cells. In order to understand more about diabetes we need to understand the mechanisms governing β-cell death.</p><p>The leukemia drug Gleevec is a tyrosine kinase inhibitor that targets c-Abl. Surprisingly, Gleevec also counteracts Type 2 diabetes and acts as a cell death inhibiting agent, via inhibition c-Abl. Since both Type 1 and Type 2 diabetes are characterized by an increased β-cell death, and the role of c-Abl is unknown in β-cells, we wanted to investigate the following:</p><p>1.Does Gleevec act via inhibition of c-Abl in β-cells?</p><p>2.Can Gleevec treatment prevent beta-cell death and diabetes? </p><p>3.Which downstream signaling pathways are affected by Gleevec?</p><p>In paper I, in order to determine whether Gleevec acts by inhibiting c-Abl, we used RNA-interference. Interestingly, siRNA against c-Abl produced by recombinant Dicer mediate almost complete and non-toxic silencing of c-Abl mRNA in dispersed islet cells and conferred protection from streptozotocin and cytokines.</p><p>In paper II we show that Gleevec protects β-cells from nitric oxide, pro-inflammatory cytokines and streptozotocin in vitro and that Gleevec can prevent diabetes development in the NOD mouse and the streptozotocin-injected mouse. We also present the hypothesis that Gleevec induces a state resembling ischemic preconditioning.</p><p>Paper III presents an additional mechanism by which Gleevec might improve β-cell survival, i.e. via the inhibition of the downstream stress-activated protein kinase c-Jun N-terminal kinase (JNK), the activity of which has been implicated in β-cell death signaling pathways. </p><p>In paper IV we explore the interactions between the adaptor protein Shb and c-Abl. We presently show an association between Shb-c-Abl and that Shb is a substrate for the c-Abl kinase that might regulate stress-induced c-Abl activity.</p>

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Type 1 Diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing beta cells in the pancreas. Amelioration of T1D and the prevention of its detrimental complications are possible through islet transplantation, wherein hormone-producing clusters of cells, islets of Langerhans (islets), are separated from the pancreas and transplanted into a diabetic patient. However, alterations due to the effects of organ recovery, cold ischemia time (CIT), and islet isolation may increase the inflammatory and immunogenic properties of these islets, thereby predisposing them to functional impairment and rejection in a transplant. Understanding the inflammatory properties of islets will allow for the development of strategies that decrease early islet loss and effectively enhance engraftment and long-term function. Therefore, the aims of this study were to 1) identify and characterize populations of antigen presenting cells (APC) and other immune cells in nonhuman primate (NHP) islets in situ and after isolation; and 2) characterize the expression and functional role of CD40 and the IFN alpha receptor in NHP islets, including their effects on islet immunogenicity. A surprising result of these studies was that half of the APC present in isolated NHP islets were B lymphocytes. We observed that the number of islet-resident immune cells increased with islet size, and described the localization pattern of these cells within islets. We characterized CD40 expression in NHP islets, demonstrating that multiple CD40 isoforms are expressed, and made the novel finding that functional CD40 is expressed on the somatostatin-producing δ cells. When CD40 was stimulated with its ligand, it induced downstream signaling changes, increased proinflammatory cytokine release, and increased islet immunogenicity. Based on our results, we have hypothesized a model of CD40 signaling in islet δ cells. Microarray analysis revealed expression changes in many inflammatory molecules integral to inflammation, the immune response, and apoptosis in islets that had endured increased CIT, demonstrating the unfavorable conditions created within islets following organ recovery, CIT, and islet isolation. Furthermore, we demonstrated that the IFN alpha receptor is present on isolated NHP islets, and that stimulation with IFN alpha leads to increased proinflammatory cytokine release, surface receptor upregulation, and a decrease in immunogenicity. In summary, in NHP islets we have defined the type and quantity of immune cells, the inflammatory molecules expressed, including CD40 and the IFN alpha receptor, and their downstream functional roles in an immune response.

Thesis (Ph. D.)--University of Texas at Austin, 2006. / Vita. Includes bibliographical references.

Thesis (Ph. D.)--Oregon State University, 2007. / Printout. Includes bibliographical references (leaves 124-140). Also available on the World Wide Web.

Diabetic rats exhibit decrease in plasma arginine, NO synthesis and tetrahydrobiopterin in endothelial cells (EC). Treatment with L-arginine may be beneficial for enhancing NO synthesis in diseases associated with endothelial dysfunction. However, little is known about the mechanism responsible for the stimulatory effect of arginine on endothelial NO synthesis. We hypothesized that dietary arginine supplementation increases BH4 for NO synthesis in EC of diabetic rats, thereby preventing endothelial dysfunction. In experiment I, streptozotocin (STZ) induced-diabetic male Sprague Dawley (SD) rats (a model of type-I diabetes) were individually pair-fed a casein-based diet on the basis of feed intake (per kg body weight) of non-diabetic SD rats. Addition of arginine-HCl or alanine to drinking water for the rats were adjusted daily to ensure isonitrogenous provision per kg body weight. In non-diabetic rats, arginine supplementation increased plasma arginine (144%), plasma insulin (44%), EC arginine (88%), EC BH4 (106%) and EC NO synthesis (80%), compared with alanine treatment. In diabetic rats, arginine supplementation reduced body weight loss (36%), and plasma glucose (54%), and increased plasma arginine (110%), plasma insulin (209%), EC arginine (173%), EC BH4 (128%) and EC NO synthesis (125%), compared with alanine treatment. In experiment II, male Zucker diabetic fatty (ZDF) rats (a model of type-II diabetes) were individually pair-fed a Purina 5008 diet on the basis of feed intake by alanine-treated diabetic rats (per kg body wt). Addition of arginine-HCl or alanine to drinking water for the rats was adjusted daily to ensure isonitrogenous provision per kg body weight. Arginine supplementation to ZDF rats did not affect plasma glucose and insulin, reduced epidididmal fat (30%), abdominal fat (43%) and body weight gain (18%), and increased plasma arginine (273%), EC arginine (197%), EC BH4 (120%) and EC NO synthesis (122%), compared with alanine-treated ZDF rats. These results show that dietary L-arginine supplementation increases BH4 and NO synthesis in EC of both STZ-diabetic and ZDF rats. Strikingly, arginine treatment prevented hyperglycemia in STZ-diabetic SD rats and reduced obesity in ZDF rats. Collectively, results demonstrate that oral administration of arginine is beneficial for both type-I and type-II diabetic rats.

<p>Increasing diabetes prevalence rates, poor involvement of and limited knowledge among health care professionals in disease management, and poor implementation of guidelines are barriers to quality diabetes care. This thesis aimed to develop, implement and evaluate an on-site diabetes pharmacotherapy program for public sector pharmacists. Qualitative and quantitative research methods were used inthe pre- and post-intervention study.</p>