Dental Education Economics: Challenges and Innovative Strategies

This article reviews current dental education economic challenges such as increasing student tuition and debt, decreasing funds for faculty salaries and the associated faculty shortage, and the high cost of clinic operations and their effect on the future of dentistry. Management tactics to address these issues are also reviewed. Despite recent efforts to change the clinical education model, implementation of proposed faculty recruitment and compensation programs, and creation of education- corporate partnerships, the authors argue that the current economics of public dental education is not sustainable. To remain viable, the dental education system must adopt transformational actions to re-engineer the program for long-term stability. The proposed re-engineering includes strategies in the following three areas: 1) educational process redesign, 2) reduction and redistribution of time in dental school, and 3) development of a regional curriculum. The intent of these strategies is to address the financial challenges, while educating adequate numbers of dentists at a reasonable cost to both the student and the institution in addition to maintaining dental education within research universities as a learned profession

LONG-TERM METABOLIC AND HORMONAL EFFECTS OF EXENATIDE ON ISLET TRANSPLANT RECIPIENTS WITH ALLOGRAFT DYSFUNCTION: 1318

The initial success of islet transplantation (ITx) is followed by graft dysfunction (GDF) and insulin reintroduction. Exenatide, a GLP-1 agonist, increases insulin and decreases glucagon secretion and has potential for β-cell regeneration. To improve functional islet mass, exenatide treatment was given to ITx recipients with GDF. The objective of this study was to assess metabolic and hormonal effects of exenatide in GDF. In this prospective, single-arm, nonrandomized study, 11 type 1 diabetes recipients of ITx with GDF had HbA1c, weight, insulin requirements, and 5-h mixed meal tolerance test (MMTT; with/without exenatide given before test) at baseline, 3, 6, and 12 months after initiating exenatide treatment. Baseline MMTT showed postprandial hyperglycemia and hyperglucagonemia. Daily exenatide treatment resulted in improved glucose, increased amylin/insulin ratio, and decreased proinsulin/insulin ratio as assessed by MMTT. Glucagon responses remained unchanged. Exenatide administration 1 h before MMTT showed decreased glucagon and glucose at 0 min and attenuation in their postprandial rise. Time-to-peak glucose was delayed, followed by insulin, proinsulin, amylin, and C-peptide, indicating glucose-driven insulin secretion. Five subjects completed 12-month follow-up. Glucose and glucagon suppression responses after MMTT with exenatide were no longer observed. Retrospective 3-month analysis of these subjects revealed higher and sustained glucagon levels that did not suppress as profoundly with exenatide administration, associated with higher glucose levels and increased C-peptide responses. In conclusion, Exenatide suppresses the abnormal postprandial hyperglucagonemia and hyperglycemia observed in GDF. Changes in amylin and proinsulin secretion may reflect more efficient insulin processing. Different degrees of responsiveness to exenatide were identified. These may help guide the clinical management of ITx recipients

Morphological study of the anatomical variations of anterior belly of digastric muscle in Brazilian cadavers

Background: Cases of variations in anterior belly of the digastric muscle must be carefully identified to avoid misinterpretations and assist in the correct surgical or aesthetic procedure and help in the teaching of Anatomy. The aim of this study was to describe the anatomical variations of anterior belly of digastric muscle in Brazilian cadavers. Materials and methods: Thirty-one human heads were selected, from adult cadavers (18 to 80 years, 29 males and 2 females). The morphology of the anterior belly of the digastric muscle was observed, identifying the possible anatomical variations that were characterized and classified according to the amount of muscle bellies, fiber direction and place of origin and insertion. The morphometric measurements were performed using a digital caliper. To analyze the data obtained, photographic documentation, anatomical description and individual morphometric description of each muscle belly were performed. The incidence of anatomical variation was obtained in percentage (%). Results: The anatomical variation of the anterior belly of the digastric muscle was present in 6 cadavers (19.31%; 1 female and 5 male). All anatomical variations presented an accessory belly to the anterior belly. However, these accessory bellies were configured differently in the location, direction of muscle fibers and in their dimensions (length and width). Conclusions: The gross anatomy of the anterior belly of the DM and their variations is important to assist in surgical procedures, pathological or diagnostic function. In addition, asymmetrical variations in the submental region must be carefully identified to avoid misinterpretations

Recurrence of Type 1 Diabetes After Simultaneous Pancreas-Kidney Transplantation, Despite Immunosuppression, Is Associated With Autoantibodies and Pathogenic Autoreactive CD4 T-Cells

ObjectiveTo investigate if recurrent autoimmunity explained hyperglycemia and C-peptide loss in three immunosuppressed simultaneous pancreas-kidney (SPK) transplant recipients.Research design and methodsWe monitored autoantibodies and autoreactive T-cells (using tetramers) and performed biopsy. The function of autoreactive T-cells was studied with in vitro and in vivo assays.ResultsAutoantibodies were present pretransplant and persisted on follow-up in one patient. They appeared years after transplantation but before the development of hyperglycemia in the remaining patients. Pancreas transplant biopsies were taken within approximately 1 year from hyperglycemia recurrence and revealed beta-cell loss and insulitis. We studied autoreactive T-cells from the time of biopsy and repeatedly demonstrated their presence on further follow-up, together with autoantibodies. Treatment with T-cell-directed therapies (thymoglobulin and daclizumab, all patients), alone or with the addition of B-cell-directed therapy (rituximab, two patients), nonspecifically depleted T-cells and was associated with C-peptide secretion for >1 year. Autoreactive T-cells with the same autoantigen specificity and conserved T-cell receptor later reappeared with further C-peptide loss over the next 2 years. Purified autoreactive CD4 T-cells from two patients were cotransplanted with HLA-mismatched human islets into immunodeficient mice. Grafts showed beta-cell loss in mice receiving autoreactive T-cells but not control T-cells.ConclusionsWe demonstrate the cardinal features of recurrent autoimmunity in three such patients, including the reappearance of CD4 T-cells capable of mediating beta-cell destruction. Markers of autoimmunity can help diagnose this underappreciated cause of graft loss. Immune monitoring during therapy showed that autoimmunity was not resolved by the immunosuppressive agents used

SIRT3 controls brown fat thermogenesis by deacetylation regulation of pathways upstream of UCP1.

Objective Brown adipose tissue (BAT) is important for thermoregulation in many mammals. Uncoupling protein 1 (UCP1) is the critical regulator of thermogenesis in BAT. Here we aimed to investigate the deacetylation control of BAT and to investigate a possible functional connection between UCP1 and sirtuin 3 (SIRT3), the master mitochondrial lysine deacetylase.Methods We carried out physiological, molecular, and proteomic analyses of BAT from wild-type and Sirt3KO mice when BAT is activated. Mice were either cold exposed for 2 days or were injected with the β3-adrenergic agonist, CL316,243 (1 mg/kg; i.p.). Mutagenesis studies were conducted in a cellular model to assess the impact of acetylation lysine sites on UCP1 function. Cardiac punctures were collected for proteomic analysis of blood acylcarnitines. Isolated mitochondria were used for functional analysis of OXPHOS proteins.Results Our findings showed that SIRT3 absence in mice resulted in impaired BAT lipid use, whole body thermoregulation, and respiration in BAT mitochondria, without affecting UCP1 expression. Acetylome profiling of BAT mitochondria revealed that SIRT3 regulates acetylation status of many BAT mitochondrial proteins including UCP1 and crucial upstream proteins. Mutagenesis work in cells suggested that UCP1 activity was independent of direct SIRT3-regulated lysine acetylation. However, SIRT3 impacted BAT mitochondrial proteins activities of acylcarnitine metabolism and specific electron transport chain complexes, CI and CII.Conclusions Our data highlight that SIRT3 likely controls BAT thermogenesis indirectly by targeting pathways upstream of UCP1