Managers' role in maximising investment in continuing professional education.

Healthcare organisations face the challenge of delivering care in increasingly complex environments. To do so they depend on competent professionals, and continuing professional education (CPE) plays a major part in ensuring that staff maintain and develop their knowledge and skills. However, there is limited evidence of the effect of CPE on healthcare outcomes, and an emphasis on outcomes has overlooked the contribution of the processes that underlie effective CPE. This article reports the results of a study that explored a range of stakeholders' perceptions of the processes that maximise the positive effects of CPE on practice. Analysis of results shows that CPE can help improve care when supported by positive organisational cultures, effective partnership working between stakeholders and supportive learning environments that enable individuals to maximise their learning. This article discusses how managers play a pivotal role in creating positive cultures in which CPE can flourish by being role models and change agents, ensuring organisational strategic objectives are aligned with personal development plans, and by working collaboratively with education colleagues to ensure that learning from CPE is embedded in practice.

Practice makes perfect: tips for successful institutional review board submissions.

As the nursing profession seeks to develop evidence-based practice, nurses are being encouraged to embark on research in their institutions. Staff nurses and nurse clinicians often struggle with the process of obtaining institutional review board approval for their projects. When classes are available, the focus is frequently on informing nurses about the federal regulations for protection of human subjects. This article addresses practical strategies for addressing these regulations from the perspective of both the individual nurse and the nursing leader.

Teaching about genetic testing issues in the undergraduate classroom: a case study.

Educating undergraduates about current genetic testing and genomics can involve novel and creative teaching practices. The higher education literature describes numerous pedagogical approaches in the laboratory designed to engage science and liberal arts students. Often these experiences involve students analyzing their own genes for various polymorphisms, some of which are associated with disease states such as an increased risk for developing cancer. While the literature acknowledges possible ethical ramifications of such laboratory exercises, authors do not present recommendations or rubrics for evaluating whether or not the testing is, in fact, ethical. In response, we developed a laboratory investigation and discussion which allowed undergraduate science students to explore current DNA manipulation techniques to isolate their p53 gene, followed by a dialogue probing the ethical implications of examining their sample for various polymorphisms. Students never conducted genotyping on their samples because of ethical concerns, so the discussion served to replace actual genetic testing in the class. A basic scientist led the laboratory portion of the assignment. A genetic counselor facilitated the discussion, which centered around existing ethical guidelines for clinical genetic testing and possible challenges of human genotyping outside the medical setting. In their final papers, students demonstrated an understanding of the practice guidelines established by the genetics community and acknowledged the ethical considerations inherent in p53 genotyping. Given the burgeoning market for personalized medicine, teaching undergraduates about the psychosocial and ethical dimensions of human gene testing seems important and timely, and introduces an additional role genetic counselors can play in educating consumers about genomics.

State of Delaware response to novel H1N1 influenza: Division of Public Health's perspective.

The novel H1N1 influenza in 2009 and 2010 demonstrated the important relationship between medicine and public health. Delaware physicians may benefit from knowing how the state Division of Public Health (DPH) responded. One way to describe that response is to compare H1N1 influenza activities to the Ten Essential Public Health Services, adopted as standard practice by most public health agencies.

Actinobacillus actinomycetemcomitans lipopolysaccharide-mediated experimental bone loss model for aggressive periodontitis.

BACKGROUND: Bacterial constituents, such as Gram-negative derived lipopolysaccharide (LPS), can initiate inflammatory bone loss through induction of host-derived inflammatory cytokines. The aim of this study was to establish a model of aggressive inflammatory alveolar bone loss in rats using LPS derived from the periodontal pathogen Actinobacillus actinomycetemcomitans. METHODS: Eighteen female Sprague-Dawley rats were divided into LPS test (N = 12) and saline control (N = 6) groups. All animals received injections to the palatal molar gingiva three times per week for 8 weeks. At 8 weeks, linear and volumetric alveolar bone loss was measured by micro-computed tomography (microCT). The prevalence of inflammatory infiltrate, proinflammatory cytokines, and osteoclasts was assessed from hematoxylin and eosin, immunohistochemical, or tartrate-resistant acid phosphatase (TRAP)-stained sections. Statistical analysis was performed. RESULTS: A. actinomycetemcomitans LPS induced severe bone loss over 8 weeks, whereas control groups were unchanged. Linear and volumetric analysis of maxillae by microCT indicated significant loss of bone with LPS administration. Histologic examination revealed increased inflammatory infiltrate, significantly increased immunostaining for interleukin IL-6 and -1beta and tumor necrosis factor-alpha, and more TRAP-positive osteoclasts in the LPS group compared to controls. CONCLUSION: Oral injections of LPS derived from the periodontal pathogen A. actinomycetemcomitans can induce severe alveolar bone loss and proinflammatory cytokine production in rats by 8 weeks.

A p38 mitogen-activated protein kinase inhibitor arrests active alveolar bone loss in a rat periodontitis model.

BACKGROUND: Gram-negative bacterial species, such as Actinobacillus actinomycetemcomitans, contain lipopolysaccharide (LPS) that initiates the innate immune system, resulting in inflammatory alveolar bone loss. LPS activates Toll-like receptors on membrane surfaces, stimulating many intracellular signaling cascades, including the p38 mitogen-activated protein kinase (MAPK). Activation of p38 signaling mediates inflammatory cytokine expression, contributing toward osteoclastogenesis and bone loss. The aim of this study was to determine whether the novel, orally active p38 MAPK inhibitor SD282 could arrest progression of LPS-induced alveolar bone destruction in rats. METHODS: Three groups of female Sprague-Dawley rats received LPS injections to the palatal molar gingiva three times per week for 4 weeks to establish periodontitis. From weeks 5 through 8, two groups received the drug SD282 (N = 14) or 1% polyethylene glycol drug vehicle (N = 14) via oral gavage in addition to LPS injections. The third group continued to receive only LPS injections (N = 8). Microcomputed tomography was used to measure volumetric alveolar bone loss, expressed as bone volume fraction (BVF). Expression of interleukin (IL)-1 and -6 and tumor necrosis factor-alpha (TNF-alpha) was assessed by immunohistochemistry, and osteoclasts were enumerated by tartrate-resistant acid phosphatase staining. RESULTS: By 4 weeks, severe alveolar bone resorption was seen in LPS-injected animals. Administration of SD282 significantly blocked additional volumetric bone loss in the LPS-only versus LPS + SD282 groups (0.37 +/- 0.01 BVF versus 0.43 +/- 0.01 BVF; P < 0.01). Significant reductions in IL-1beta (P < 0.01 ), TNF-alpha (P < 0.05), and osteoclast formation (P < 0.01) occurred in the presence of SD282. CONCLUSIONS: An orally active p38 MAPK inhibitor reduced LPS-induced inflammatory cytokine expression, osteoclastogenesis, and alveolar bone loss in rats. Within the limits of the current study, SD282 arrested periodontal disease progression, thus highlighting the therapeutic potential of this novel class of inhibitors.

Illuminating the process: enhancing the impact of continuing professional education on practice.

BACKGROUND: There has been significant global investment in continuing professional education (CPE) to ensure healthcare professionals have the knowledge and skills to respond effectively to the needs of patients/service users. However, there is little evidence to demonstrate that this investment has had a tangible impact on practice. Furthermore, the current emphasis on evaluating outcomes has overlooked the importance of underlying processes which, when positive, are essential to good outcomes. OBJECTIVE: The aim of this study was to identify the processes that key stakeholders perceive to be most important in facilitating a positive impact of CPE on practice. DESIGN/METHOD: A qualitative design using two rounds of semi-structured interviews which were recorded and transcribed prior to analysis, informed by template analysis techniques. SETTING: Two acute trusts, one primary care trust and two higher education institutions in one geographical region in England. PARTICIPANTS: Representatives from four stakeholder groups-students, managers, educators and members of each healthcare organisation's governing board. A total of 35 interviews were conducted in the first round and 31 interviews in the second round (n=66). RESULTS: Four overarching themes were identified that illuminate stakeholders' perspectives of the important factors affecting the process of CPE: organisational structure, partnership working, a supportive learning environment and changing practice. CONCLUSIONS: This study suggests that a positive organisational culture, effective partnership working between key stakeholders with an understanding of each other's perspectives, aspirations and constraints, and a supportive learning environment in both the practice setting and education environment are central to establishing a culture and context where CPE can thrive and exert a positive influence on improving patient/service user experience and care. It is argued that an understanding of the processes that facilitate effective CPE is a crucial first step before it is possible to meaningfully evaluate outcomes.

The ethical implications of genetic testing in the classroom.

The development of classroom experiments where students examine their own DNA is frequently described as an innovative teaching practice. Often these experiences involve students analyzing their genes for various polymorphisms associated with disease states, like an increased risk for developing cancer. Such experiments can muddy the distinction between classroom investigation and medical testing. Although the goals and issues surrounding classroom genotyping do not directly align with those of clinical testing, instructors can use the guidelines and standards established by the medical genetics community when evaluating the ethics of human genotyping. We developed a laboratory investigation and discussion which allowed undergraduate science students to explore current DNA manipulation techniques to isolate their p53 gene, followed by a dialogue probing the ethical implications of examining their sample for various polymorphisms. Students never conducted genotyping on their samples because of the ethical concerns presented in this paper, so the discussion replaced the actual genetic testing in the class. A science faculty member led the laboratory portion, while a genetic counselor facilitated the discussion of the ethical concepts underlying genetic counseling: autonomy, beneficence, confidentiality, and justice. In their final papers, students demonstrated an understanding of the practice guidelines established by the genetics community and acknowledged the ethical considerations inherent in p53 genotyping. Given the burgeoning market for personalized medicine, teaching undergraduates about the psychosocial and ethical dimensions of human genetic testing is important and timely. Moreover, incorporating a genetic counselor in the classroom discussion provided a rich and dynamic discussion of human genetic testing.

A p38alpha selective mitogen-activated protein kinase inhibitor prevents periodontal bone loss.

In the oral microbial environment, Gram-negative bacterial derived lipopolysaccharide (LPS) can initiate inflammatory bone loss as seen in periodontal diseases. p38 Mitogen-activated protein kinase (MAPK) signaling is critical to inflammatory cytokine and LPS-induced cytokine expression, which may contribute toward periodontal bone loss. The purpose of this proof-of-principle study was to evaluate the ability of an orally active p38alpha MAPK inhibitor (SD-282) to reduce periopathogenic LPS-induced alveolar bone loss in an experimental rat model. Five groups of Sprague-Dawley rats received one of the following treatments: LPS injected to the palatal gingiva adjacent to the maxillary molars three times per week for 8 weeks, LPS plus two doses of SD-282 (15 or 45 mg/kg) twice daily by oral gavage, or control groups given drug vehicle (1% polyethylene glycol) or SD-282 (45 mg/kg) only. Baseline and 8-week alveolar bone loss was assessed by microcomputed tomography (microCT) and histological examination. LPS induced severe bone loss over this time period, whereas control groups were unchanged from baseline measurements. Both doses of SD-282 showed significant protection from LPS-induced bone loss. Bone area and volumetric analysis of maxillas by microCT indicated significant loss of bone volume with LPS treatment, which was blocked with the p38 inhibitor. Histological examination indicated significantly fewer tartate-resistant acid phosphatase-positive osteoclasts and a significant decrease in interleukin (IL)-6, IL-1beta, and tumor necrosis factor alpha expression in p38 inhibitor-treated groups compared with LPS groups by immunostaining. Results from this in vivo study suggest that orally active p38 MAPK inhibitors can reduce LPS-induced inflammatory cytokine production and osteoclast formation and protect against LPS-stimulated alveolar bone loss.