6 полученные результаты
A group of poorly studied immune-mediated neurological syndromes are associated with antibodies against glutamic-acid decarboxylase (GAD-Ab). GAD is the rate-limiting enzyme for the synthesis of gamma aminobutyric acid (GABA) from glutamate and is expressed by inhibitory neurons of the central
The primary defect in autoimmune Type I Diabetes Mellitus (T1DM) involves the infiltration of the pancreatic islet cells by T-lymphocytes, macrophages, and other immune cells, and consequent loss of beta cells. At the onset of T1DM more than 70% of the beta cells are destroyed, whereas the residual
Primary Outcome:
The primary statistical hypothesis to be assessed in this study is whether the mean C-peptide value for study subjects receiving GABA differs significantly from the mean value for placebo subjects assessed at follow-up.
Secondary Outcome:
The study will examine the HbA1C and the
Adult-onset latent autoimmune diabetes (LADA), etiologically belongs to type 1 diabetes (T1D), is characterized by the presence of islet autoantibodies, such as islet cell antibody (ICA) and glutamic acid decarboxylase antibody (GADA), and is prone to develop β-cell failure. The goals of treatment
Type 1 diabetes mellitus (T1D) is caused by autoimmune and autoinflammatory destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans. Historically, treatment for this condition has consisted of insulin replacement therapy and dietary modification. Recent studies have
Type 1 diabetes and Type 2 diabetes have different underlying pathophysiologic processes. The disease process in classical Type 1 diabetes is an autoimmune destruction of the pancreatic beta cells. In contrast, the disease process in classical Type 2 diabetes is not autoimmune in nature, a decreased