Nixonmoon2434

05). Protein intake ratio (DHQ/24-h urine) was positively associated with duration of diabetes only in men (p  less then  0.05); however, this relation disappeared in the multivariable model. No factors showed association with sodium or potassium intake ratio. The DHQ showed under-reporting of energy intake by approximately 15% in Japanese patients with T2D. This was associated with obesity in both sexes and with younger age in women.

People with diabetes need to make regular choices that influence their long-term morbidity and mortality. Patient decision aids are validated tools and when used collaboratively between healthcare professionals, patients and carers, can help guide value-based discussions which encourage choices that are well informed and personally relevant.

To explore the use and effect of patient decision aids in the management of diabetes.

A scoping review design was used. Medline, ProQuest, PsycINFO, Scopus, and Cumulative Index to Nursing and Allied Health Literature databases were searched for peer-reviewed articles published between January 1998 and December 2018.

Patient decision aids are not commonly or widely used in diabetes management. They offer a suitable adjunct to practice within the domains of healthcare knowledge, active participation, and communication, and shared decision-making between patients and healthcare professionals.

Patient decision aids can offer a simple and easy-to-use method to potentially improve diabetes health literacy, through the process of shared decision-making and two-way conversations. However, there are current limitations on using them to positively influence clinical outcomes or long-term changes in self-care behaviors within the management of diabetes. Further research to explore the validity of using patient decision aids long term in these areas is required.

Patient decision aids can offer a simple and easy-to-use method to potentially improve diabetes health literacy, through the process of shared decision-making and two-way conversations. However, there are current limitations on using them to positively influence clinical outcomes or long-term changes in self-care behaviors within the management of diabetes. Further research to explore the validity of using patient decision aids long term in these areas is required.To clarify the clinical and etiological characteristics of fulminant type 1 diabetes, we reviewed data from patients who had developed type 1 diabetes following anti-programmed cell death 1/programmed cell death ligand 1 (anti-PD-1/PD-L1) therapy, and research on pancreatic beta cells derived from induced pluripotent stem (iPS) cells from patients with fulminant type 1 diabetes. As determined from the disease classifications and clinical and genetic characteristics, anti-PD-1/PD-L1 therapy-related type 1 diabetes includes both fulminant type 1 diabetes and acute-onset type 1 diabetes. Using insulin-positive cells derived from iPS cells, beta-cell fragility to inflammatory cytokines, but not its regeneration failure, was observed in fulminant type 1 diabetes. Moreover, severe hyperglycemia was reported as a risk factor of sudden death or cardiac arrest at disease onset, diffusion-weighted magnetic resonance imaging was suggested as an additional tool for making a diagnosis, and the CSAD/lnc-ITGB7-1 locus was genetically associated with fulminant type 1 diabetes. To fully understand fulminant type 1 diabetes, it is important to clarify the molecular mechanisms step by step through multifaceted approaches such as through analyses of the genetic factors, clinical features, histological findings, and cell biology. The careful and detailed study of patients is a great means for clarifying the etiology and pathophysiology of the disease.Fulminant type 1 diabetes (FT1D) is characterized by a relatively low HbA1c level at the onset, despite the abrupt occurrence of marked hyperglycemia with ketosis or ketoacidosis. The initial symptoms/findings are flu-like, absence of islet-associated autoantibodies, and a drastic decrease in β-cells and α-cells, which strongly suggest the involvement of a viral infection. GSK-2879552 molecular weight In fact, we successfully demonstrated that a FT1D-like phenotype can be reproduced in encephalomyocarditis virus-induced diabetes murine model. However, there is a discussion on the possible involvement of autoimmunity rather than viral infection as the underlying cause of FT1D. For example, HLA-DRB1*0405, a susceptible antigen of type 1A diabetes, is reportedly associated with FT1D in Japan. Moreover, anti-glutamic acid decarboxylase antibody is reportedly detected in ~ 5% of the patients. Additionally, half of the patients with anti-programmed cell death-1 therapy-related type 1 diabetes fulfilled the criteria of the disease. These findings suggest that islet-associated autoimmunity can partially contribute to the development of FT1D. Furthermore, using nonobese diabetic mice with reduced regulatory T-cell (Treg) numbers, we found that a human FT1D-like phenotype can be induced by islet-associated autoimmunity through collaboration between innate immunity (macrophages and/or natural killer cells) and acquired immunity (predominantly cytotoxic CD8+ T cells) in genetically predisposed individuals of autoimmune type 1 diabetes with low Tregs or Treg dysfunction. To clarify greater details regarding the association of autoimmunity in the pathogenesis of FT1D, further studies using suitable animal models and accumulation of the relevant patients are required.Distinct features of the pancreas of fulminant type 1 diabetes (FT1DM) include (1) enterovirus infection of the islets and exocrine acinar tissue. (2) Activated innate immune responses MDA5 and RIG-I expression and TLR4 and TLR9 expression in the islets of FT1DM. (3) Combined activation of the STAT/JNK and NFkB pathways, resulting in Type I interferon (IFN) and proinflammatory cytokine (i.e., IFNγ) expression in islet beta cells and MHC class I hyper-expression. (4) Activation of dendritic cells followed by effector cell infiltration of CD8+ T cells and CD68+ macrophages, resulting in apoptosis and neurosis of islet cells and exocrine acinar cells. (5) Many chemo-attractants (i.e., CXCL10) and chemotactic activators (i.e., l-plastin) were induced by a viral infection. (6) Mutual stimulating effect of cytokines expressed in beta cells in autocrine and paracrine mechanisms may enhance beta-cell destruction through the STA1-caspase pathway. (7) Proteomics analysis using laser capture microdissection followed by mass spectrometry found 38 molecules in inflamed islets of FT1DM, which were not highlighted before.