ABSTRACT
INTRODUCTION: In addition to understanding core public health fundamentals, health professionals must also be equipped with the skills necessary to implement strategies to promote population health. In response, the University of New Hampshire (UNH) has developed a unique Public Health Certificate (PHC) Program designed to strengthen knowledge and skills in basic public health competencies of working health professionals. A distinctive feature of this program is its culminating course "Applied Topics in the Essentials of Public Health," which entails a practical, applied learning experience where students explore a variety of essential public health services (EPHS) relevant to their career goals. OBJECTIVES: 1) Explain the rationale for educating working health professionals about public health; 2) Describe the UNH graduate PHC Program, its framework and innovative process for implementing a skills-based course to improve the competency of practitioners to perform the EPHS; 3) Review the benefits and challenges of implementing a skills-based course for working health professionals; and 4) Evaluate the PHC Program. DISCUSSION: The UNH PHC Program and its capstone course serve as a model for providing a unique, skills-based learning opportunity for working health professionals pursuing advanced public health education in U.S.-based or international public health education programs. This novel course design allows for students to develop the skills necessary to perform the EPHS.
Subject(s)
Certification/organization & administration , Health Personnel/education , Professional Competence/standards , Public Health Practice , Education , Humans , New Hampshire , Organizational Case Studies , Program DevelopmentABSTRACT
Previous studies in our laboratory have demonstrated that genotoxic chemical carcinogens have strong preferential effects on expression of certain inducible genes at nonovertly toxic doses in vivo. The effects of the DNA cross-linking agent and chemotherapy drug, mitomycin C (MMC), on expression of the developmental and hormone-regulated gene, phosphoenolpyruvate carboxykinase (PEPCK), were examined in chick embryo liver in vivo as a function of development and were compared with changes in the chromatin structure of the PEPCK gene promoter. The liver PEPCK gene was fully hormone inducible as early as 8 days of embryonic development but was refractory to MMC until after day 10. This onset of responsiveness to MMC was correlated with qualitative changes in the pattern of DNase I hypersensitive sites (DHS) within the PEPCK promoter. There was also a gradual decrease and then a complete loss of both hormone inducibility and MMC responsiveness between 14 and 17 days of development that was correlated with a quantitative change in the overall DNase sensitivity of the liver PEPCK gene promoter over this period. These results suggest that carcinogen sensitivity of the PEPCK gene is related to its ability to respond to its normal induction signals and that chromatin structure may play a central role in these effects.
Subject(s)
Chromatin/chemistry , Gene Expression Regulation, Developmental/drug effects , Gene Expression Regulation, Enzymologic/drug effects , Mitomycin/pharmacology , Phosphoenolpyruvate Carboxykinase (ATP)/genetics , Promoter Regions, Genetic , Animals , Antineoplastic Agents, Alkylating/pharmacology , Chick Embryo , Protein Conformation , RNA, Messenger/geneticsSubject(s)
Chromosomes/radiation effects , Mutagenesis/genetics , Neoplasms, Radiation-Induced/genetics , Animals , CHO Cells , Cell Transformation, Neoplastic/genetics , Chromosome Aberrations , Cricetinae , DNA Damage , Gene Deletion , Gene Expression Regulation , Genes, Tumor Suppressor/genetics , Genome , Genome, Human , Humans , Mutagenesis/radiation effects , Mutation/genetics , Oncogenes/genetics , Point Mutation/genetics , Signal Transduction/geneticsABSTRACT
The immediate effects of a single dose of the chemotherapeutic DNA crosslinking agent, mitomycin C (MMC), on the expression of several constitutive and drug-inducible genes were examined in a simple in vivo system, the 14 day chick embryo. We observed no effect of MMC on the steady-state mRNA expression of the constitutively expressed beta-actin, transferrin, or albumin genes. In contrast, MMC treatment significantly altered both the basal and drug-inducible mRNA expression of two glutethimide-inducible genes, 5-aminolevulinic acid (ALA) synthase and cytochrome P450 CYP2H1. The basal expression of these genes was transiently but significantly increased over a 24 hr period following a single dose of MMC. Conversely, MMC significantly suppressed the glutethimide-inducible expression of these genes when administered 1 to 24 hr prior to the inducing drug. The effects of MMC on both basal and drug-inducible ALA synthase and CYP2H1 mRNA expression were principally a result of changes in the transcription rates of these genes. In contrast, MMC treatment had little or no effect on glutethimide-induced expression of ALA synthase or CYP2H1 when administered 1 hr after the inducing drug, suggesting that a very early event in the induction process represents the target for these MMC effects. Covalent binding studies demonstrated that the effects of MMC on gene expression were closely correlated temporally with formation of [3H]-porfiromycin-DNA adducts. These results support the hypothesis that genotoxic chemicals specifically target their effects to inducible genes in vivo.
