RESUMEN
A local safety net clinic provides pharmacy directed Diabetes Disease Management (DDM). The purpose of the study was to determine if a program like this would be successful in an underserved, uninsured poor minority population. Clinic providers referred patients to the DDM visits. Body Mass Index (BMI), low-density lipoprotein, high-density lipoprotein (HDL), triglycerides and hemoglobin A1c (HbA1c) were recorded pre- and post-intervention. Those who participated in pre-intervention and post-intervention visit were included in the study and laboratory values were compared. Participants in the pilot study showed statistically significant improvements in HbA1c, triglycerides and BMI. HDL values did not show statistical change. Pharmacy directed DDM can be effective in the reduction of HbA1c and triglycerides. It also may be an effective weight loss intervention for patients with diabetes.
Asunto(s)
Diabetes Mellitus/etnología , Diabetes Mellitus/terapia , Área sin Atención Médica , Pacientes no Asegurados/estadística & datos numéricos , Grupos Minoritarios/estadística & datos numéricos , Mejoramiento de la Calidad , Biomarcadores/sangre , Índice de Masa Corporal , Diabetes Mellitus/sangre , Femenino , Florida , Hemoglobina Glucada/análisis , Humanos , Lípidos/sangre , Masculino , Persona de Mediana Edad , Proyectos PilotoRESUMEN
Alterations in lysosomal proteases have been implicated in many neurodegenerative diseases. The current study demonstrates a concentration-dependent decrease in PC12 cell viability and transient changes in cystatin C (CYSC), cathepsin B (CATB), cathepsin D (CATD) and caspase-3 following exposure to H2O2. Furthermore, activation of CATD occurred following exposure to H2O2 and cysteine protease suppression, while inhibition of CATD with pepstatin A significantly improved cell viability. Additionally, significant PARP cleavage, suggestive of caspase-3-like activity, was observed following H2O2 exposure, while inhibition of caspase-3 significantly increased cell viability compared to H2O2 administration alone. Collectively, our data suggest that H2O2 induced cell death is regulated at least in part by caspase-3 and CATD. Furthermore, cysteine protease suppression increases CATD expression and activity. These studies provide insight for alternate pathways and potential therapeutic targets of cell death associated with oxidative stress and lysosomal protease alterations.