Glycemic control among patients with physician-managed type 2 diabetes.

Outcomes for treatment, overall oral health status, and periodontal disease progression in patients with type 2 diabetes mellitus (T2DM) have been associated with glycemic control as measured by hemoglobin A1c (HbA1c) levels. Due to the high prevalence of T2DM among patient populations in the United States, this study sought to assess baseline levels of glycemic control for patients with a known diagnosis of T2DM who were under the care of a physician and to identify management solutions for these patients. All patients included in this study were prescreened to ensure that they were dentate, had been diagnosed with T2DM at least 3 months previously, were under the care of a physician for diabetes management, and had no changes to their diabetes-related medications for 3 months or more (N = 822). The patients meeting those criteria were then screened in person, and those who had moderate to severe chronic periodontitis, had at least 20 teeth, and met other inclusion/exclusion criteria were qualified to participate in the study (N = 214). After the patients fasted, a whole blood sample was drawn and subjected to HbA1c testing. The mean (SD) HbA1c for the qualified patients was 7.76% (1.79%), and the values ranged from 5.1% to 18.8%. Among the 214 qualified individuals, 150 (70.1%) had HbA1c values greater than 6.5%. Of these 150 patients, 80 (53.3%, or 37.4% of the total screened sample) presented with HbA1c values greater than 8.0%. The majority of patients with periodontitis and physician-managed T2DM did not meet ideal standards for glycemic control. Dental healthcare providers should consider consultation and/or advanced screening for diabetic patients seeking dental care.

The La protein counteracts cisplatin-induced cell death by stimulating protein synthesis of anti-apoptotic factor Bcl2.

Up-regulation of anti-apoptotic factors is a critical mechanism of cancer cell resistance and often counteracts the success of chemotherapeutic treatment. Herein, we identified the cancer-associated RNA-binding protein La as novel factor contributing to cisplatin resistance. Our data demonstrate that depletion of the RNA-binding protein La in head and neck squamous cell carcinoma cells (HNSCC) increases the sensitivity toward cisplatin-induced cell death paralleled by reduced expression of the anti-apoptotic factor Bcl2. Furthermore, it is shown that transient expression of Bcl2 in La-depleted cells protects against cisplatin-induced cell death. By dissecting the underlying mechanism we report herein, that the La protein is required for Bcl2 protein synthesis in cisplatin-treated cells. The RNA chaperone La binds in close proximity to the authentic translation start site and unwinds a secondary structure embedding the authentic AUG. Altogether, our data support a novel model, whereby cancer-associated La protein contributes to cisplatin resistance by stimulating the translation of anti-apoptotic factor Bcl2 in HNSCC cells.